In 1996, Leslie Gordon, a biologist and a pediatrics resident at a hospital in Rhode Island, gave birth to a son, Sam. For a few months, Sam seemed healthy. But Gordon and her husband, a pediatric emergency physician named Scott Berns, soon started to feel that something was wrong. Sam’s skin looked tight, shiny, and veiny. He lost hair and was hardly putting on any weight. Doctors couldn’t explain why. “It was driving me crazy,” Gordon said. “They’d say, ‘Oh, he’s small, but you guys are small, too.’ ” One evening, a colleague of Berns’s, Monica Kleinman, came over for dinner and looked across the table at Sam. “Something just clicked in my mind,” Kleinman told me. She’d seen features like Sam’s in a textbook. A few days later, she told Berns that Sam might have a rare, fatal condition called progeria. “It was one of the hardest things I’ve ever had to do,” Kleinman said. A specialist in New York confirmed the diagnosis. “Within a week, it was clear that there was nothing out there,” Gordon told me. “No research. No treatments. No hope.”
Progeria, which derives from the Greek for “early old age,” was first described in the late nineteenth century. It is a disease of rapid, brutal aging that is thought to afflict fewer than one in every four million babies. By the time children with progeria enter their teen-age years, their bodies have effectively aged eight or nine decades. They have a distinctive appearance: small, wizened, and bald, with wrinkled skin, rigid arteries, stiff joints, and weak bones. Many die of heart attacks before their fifteenth birthday. There are estimated to be about twenty people living with the condition in the U.S. and several hundred in the world.
After Sam’s diagnosis, Gordon withdrew from her residency and began to study progeria full time. She and Berns started a nonprofit, the Progeria Research Foundation, and recruited her sister, Audrey, to serve as its executive director. Gordon organized a meeting of several dozen scientists from various fields: genetics, orthopedics, immunology. “I scoured the earth for anyone who knew anything that might theoretically be useful for progeria,” she said. She also assembled an international registry of dozens of progeria patients; Sam became friends with many of them. Berns, for his part, spent a year in the federal government, working as a senior adviser to the Secretary of Transportation as part of a White House Fellowship. At a work event one evening, he met Francis Collins, then the director of the National Human Genome Research Institute, which was sequencing a complete human genome for the first time. Berns told Collins about the diagnosis, not knowing whether he would recognize the condition. In fact, Collins had once cared for a patient diagnosed as having progeria.
Collins invited the family to his home. When they visited, he tossed a Frisbee with Sam, who was now four, in the back yard. He told them that he’d try to identify the genetic culprit. “That really epitomizes who Francis is,” Gordon told me. “Here he is, in charge of the entire Human Genome Project, and at the same time he’s looking for a gene for one kid.” Collins soon tasked Maria Eriksson, a postdoc from Sweden who had recently joined his institute, to search for genes that might cause progeria. “Don’t spend more than a year on this,” he told her. “If it doesn’t work out, we’ll find something else for you to work on.”
Eriksson studied the DNA of progeria patients along with that of their parents, thinking that the condition must be a recessive trait—one that shows up in a child only when both parents have a particular genetic variation. Then, on a Saturday in 2002, about a year into her work, she called Collins. “I think I’m seeing something interesting,” she told him. Children with progeria had a mutation that their parents didn’t, she said. The condition didn’t seem to be hereditary at all but, rather, to arise from a spontaneous mutation present at birth, a C replaced by a T on chromosome 1. The human genome contains billions of letters, enough to fill hundreds of books; the disease was apparently caused by the equivalent of a single typo.
Gordon and Collins held a press conference. “This discovery is likely to shed light on the normal process of aging,” Collins announced. “It reverberates well beyond its application to progeria.” In healthy cells, a protein called lamin A helps to shape and stabilize the nucleus. But the mutation produced an abnormal, toxic version of the protein called progerin, which warped the nucleus. At first, when cells affected by progeria divide, “they don’t look so bad,” Collins told me. “But, after seven or eight passes, they look really, really bad. The nuclei are totally messed up.”
Meanwhile, Sam grew older. He developed heart disease at a young age, saw numerous doctors, and took a slew of medications. When he was a teen-ager, members of the Dave Matthews Band, which he loved, heard about his condition and invited him backstage. In high school, he played the snare drum in marching band; with its harness, the instrument weighed forty pounds, nearly as much as he did. (An engineer helped design a special apparatus so he could wear it.) He went to Disney World and, because his bones were so weak, cracked two ribs just sitting on a ride. He excelled in school and said that he wanted to be an inventor, “like Albert Einstein and Steve Jobs, combined.”
Sam became the subject of an HBO documentary called “Life According to Sam,” which was released in 2013. “I kind of deal with death a lot different than other people,” he says in the movie. “I asked my mom about one of my friends, Ory, and my mom said, ‘Oh, he passed away.’ I’m, like, ‘Oh, what about Stuart?’ She’s, like, ‘Well, he passed away.’ ‘What about Ronnie?’ ‘He died, and Mierko died.’ ” A few months before his own death, at seventeen, he gave a TEDX talk that has been viewed more than a hundred million times. His life was a happy one, he told the audience, with the authority of someone preparing to depart it. Focus on what you can control, he said. Surround yourself with good people. Keep moving forward. And never miss a party if you can help it.
Kaylee Halko was born in 2003, in a small town in Ohio. She, too, had progeria. But her experience was different from Sam’s in a crucial way: she was seven years younger. When Kaylee was four, the Progeria Research Foundation helped launch the first-ever clinical trial of a potential progeria drug, and she enrolled. Young patients took lonafarnib, which had originally been investigated as a cancer treatment. They gained weight, their hearing improved, and their arteries became more pliable. Lonafarnib interfered with a sort of chemical anchor that helps the lamin A protein target the nucleus. The drug didn’t eliminate the abnormal protein, but it seemed to reduce the damage: children taking it ultimately lived two and a half years longer.
Kaylee’s parents, Tim and Marla, also had three healthy boys. They tried to insure that Kaylee had as normal an upbringing as possible, despite the obvious challenges that she would face. As a child, she experienced instances of vicious bullying about her appearance. To this day, strangers sometimes stare and point. Others direct conversation solely toward her parents. “They talk to them like I’m not even there,” Kaylee said. “They’ll look down and say, ‘Oh, how old is she?’ ”
A decade ago, Kaylee started posting short videos on Musical.ly, a social-media platform that eventually merged with TikTok. Her parents found out only after she became internet famous; she currently has half a million followers on TikTok and more than a hundred and fifty thousand on Instagram. I was surprised that, after receiving so much undesired attention, Kaylee would want to be so public online. In the comments, a small number of people sound much like those who bullied her when she was a child. But many are supportive to the point that they go after the haters on her behalf. “Kaylee’s condition has allowed me to see, to feel, the good nature of people,” Marla told me. “I don’t think I would have seen that side of humanity as clearly if it wasn’t for Kaylee.”
Some of Kaylee’s posts simply capture moments in her life: dancing in her living room, going to a concert, watching a sunset at the beach. Others try to give people a sense of what it’s like to live with progeria. In one video, viewed more than thirty million times, she snips a single hair from her otherwise bald head. In another, a sombre ballad plays while she has a subtitled conversation with her younger self.
Young Kaylee asks about her life expectancy: “So did we beat the odds?”
Older Kaylee smiles gently. “Yeah, we’re 21.”
Then young Kaylee poses a question. Older Kaylee rolls her eyes. “No,” she answers. “Our boobs did not grow.”
Recently, Kaylee filmed a video response to an insensitive comment that someone left on one of her TikToks: “for a second I thought that was my grandma’s hands.” A screen grab of the remark appears onscreen. For a moment, it looks as though Kaylee, who is wearing a baggy yellow sweatshirt, is preparing to scold or make fun of the commenter. Then it becomes clear that someone else’s hands are protruding from the sleeves, gesticulating madly. One of her college-age friends, hidden by the sweatshirt, is pretending that her hands are Kaylee’s.
Kaylee tries to do a bit, feigning shock that anyone would think she has “old-lady hands.” But her friend’s hands move so wildly that she keeps breaking character and giggling. By the end of the video, she is laughing so hard that her eyes are full of tears.
In “Far from the Tree: Parents, Children, and the Search for Identity,” the writer Andrew Solomon defines “vertical identities” as traits or norms that are passed from parents to children, and that therefore tend to be shared and celebrated: ethnicity, religion, language, customs. Horizontal identities, in contrast, are not shared. They may flow from spontaneous genetic mutations, personal experience, environmental factors, or sheer chance; they can include disease, disability, neurodivergence, and sexual orientation. “For people who must accept a fixed external reality, the only way forward is to adjust internal reality,” Solomon writes. It takes effort to transform such traits from sources of stigma and misunderstanding to objects of tolerance or pride. Often, it takes community—something that, in the case of progeria, had to be laboriously created. The Progeria Research Foundation is aware of only about a hundred and fifty people worldwide with the condition, and the population that has had it in all of human history probably numbers in the thousands. (Progeria is formally known as Hutchinson-Gilford progeria syndrome; there are other conditions that cause premature aging, but they present differently and arise from different genetic mutations.)
When Gordon created the foundation, she worked to build connections between progeria patients and their families. She now hosts Zoom calls that are attended by a quarter of known progeria patients, who in turn sometimes organize meetups around the world. Through the foundation, Kaylee befriended three others; they called themselves the “P dawgs.” In a remarkable coincidence, one lived just a few miles away, so the group often convened in Ohio. “It was special because we could really relate,” Kaylee said. “The progressiveness of the disease. The relentlessness of it.” Over time, all of the other P dawgs died. Kaylee, who went to church intermittently as a girl, has become increasingly religious, and she told me that she expects to see her friends again. “Death is not something I want to happen,” she said. “But it doesn’t scare me, either.”
Donations to the Progeria Research Foundation—from individuals, grants, fund-raising events, and campaigns by volunteers—eventually surpassed two million dollars a year. About a decade ago, Gordon directed some of the organization’s funds to a South Korean researcher named Bum-Joon Park, who was studying how the abnormal lamin A protein attaches to the nucleus of a cell. He thought he’d identified a molecule, progerinin, that could block its effect through a different mechanism than lonafarnib. In 2021, his team published a paper showing that progerinin could reduce concentrations of the toxic protein in cells and extend the life spans of mice with progeria. In Phase I safety trials conducted with healthy adults, the drug was well tolerated, and the F.D.A. green-lighted a Phase II trial, which will measure how well it works in progeria patients. Gordon is one of its primary investigators. Monica Kleinman, who first diagnosed Gordon’s son as having progeria, is another.
In January, Kaylee travelled to Boston for the start of the trial. On a frigid evening, I met her and her mom at a sports bar near Fenway Park. Kaylee’s legs dangled from her chair; a compact wheelchair and a white Labrador were nearby. After I greeted them, the dog nuzzled my leg and sat on my foot.
“Sorry,” Kaylee said. “That’s Iris. We’re still training her.” Her voice was quiet and high-pitched, and I had to lean in to hear her over the din of the bar. She ordered chicken tenders from the kids’ menu.
A few years ago, Kaylee enrolled in a program to train as an ultrasound technician, but she was eventually told that her small size—she was three feet eight and weighed thirty-some pounds—would make the job too difficult. “Gee,” she told me. “Think you could have told me that before I spent a year of my life on this?” She took law classes at a community college but soon had a realization: “I’m actually the type of person who scrolls to the bottom of the terms and conditions and just hits Accept.” Now she was studying psychology, in the hope of working as a high-school guidance counsellor. “That’ll probably take another two years,” she said, dipping a fry in some ketchup. Kaylee, like many college students, was taking time to decide what she wanted to do with her life. But she has already exceeded the average life span of a person with progeria.
Every day, Kaylee takes half a dozen medications, many of which I prescribe to elderly patients: drugs for diabetes, high blood pressure, digestive issues, thyroid problems. A doctor had recently told Kaylee that she had worsening diabetes, so she’d sworn off sugar for the month. “He also said that my triglycerides were the highest he’s ever seen and that my ‘good cholesterol’ was the lowest,” she added. “I’m setting records.”
Kaylee has had serious joint problems since she was in high school. They started in the middle of a dance class, when she leaped into the air and landed awkwardly, dislocating her hip. In addition to several hip surgeries, she has had a major cardiac operation. She has also undergone lithotripsy, which uses shock waves to break up kidney stones. (“I don’t really count those as surgeries, since they just go in and blast them,” she told me, miming the shooting of a gun.) Once, after an operation, Kaylee’s tongue swelled so much that she struggled to breathe, possibly owing to anesthetic medications and an experimental drug she was taking. She was taken to a local hospital, where doctors said that it might be difficult to intubate her, given her size. She was airlifted to a larger hospital at the University of Michigan.
“I’m not in denial, but, if I lived my life according to the stats, I couldn’t do anything,” Kaylee told me. “For me, the best way to live is just to put it out of my mind.” She made me think of a passage from “When Breath Becomes Air,” a 2016 memoir by Paul Kalanithi, a neurosurgeon who was given a diagnosis of lung cancer. He expected to die of it, but he didn’t know when. “Tell me three months, I’d spend time with family,” he wrote. “Tell me one year, I’d write a book. Give me ten years, I’d get back to treating diseases. The truth that you live one day at a time didn’t help: What was I supposed to do with that day?”
The morning after our meal, I waited for Kaylee at the Experimental Therapeutics Unit, on the sixth floor of Boston Children’s Hospital. She arrived in jeans, an oversized pink sweater, and gold cross earrings. An energetic research assistant—a premed student who was the same age as Kaylee—led us to an exam room. I thought about the difference that one letter in their genomes had made.
A physical therapist asked Kaylee to lie face up, arms crossed over her chest, on a bed that was twice her size, and took some measurements. “Your left leg is a little shorter than your right,” the therapist announced.
“Least of my problems,” Kaylee joked.
She prepared for a six-minute walk test, a standardized assessment of a person’s aerobic fitness. “Normally, they have her use a walker when she’s having hip issues,” Marla told the therapist.
“I’ll be fine without it,” Kaylee said, and shot her a look.
“Oh, the joys of an adult child,” Marla replied.
While Kaylee finished her tests, I met Gordon in the brightly lit hospital cafeteria. She had warm hazel eyes and shoulder-length brown hair. Around us, parents tended to their children. Gordon told me about a day, many years ago, when she drew blood from a teen-age boy for a progeria biobank she’d started. He had lived with the disease long enough that his symptoms were already advanced, like Kaylee’s. As she wrapped a tourniquet around his arm, he told her, “I know this isn’t going to help me. But I want to help other kids.”
Some years ago, I cared for a teen-ager with cystic fibrosis, which is usually caused by a mutation to a gene known as CFTR. (Collins, who oversaw the discovery of the progeria gene, also helped identify CFTR in the eighties.) In healthy people, the gene codes for a protein involved in clearing respiratory secretions from the lungs, but the mutation produces a defective version. As a result, thick mucus builds up in the lungs and traps bacteria, causing infections and inflammation. My patient was in the hospital with severe pneumonia.
I prescribed a series of powerful antibiotics. A respiratory therapist fitted him with a vibrating vest to shake loose the mucus plugging his airways. Even so, he was taking rapid, shallow breaths through an oxygen mask, and we knew that the strain would ultimately exhaust him. When I explained that the next step was to place him on a ventilator, he stared at me with recognition and resignation—the look of someone who had heard such explanations many times in his short life. While he was being intubated and wheeled to the I.C.U. on a stretcher, I had a wrenching feeling that I had nothing to offer him. (He went home a week later but was back in the hospital with pneumonia the next month.)
“It’s too damn slow,” Gordon told me, of the pace of research into rare diseases. “Kids are dying. Every day, I think, Why didn’t I go faster? Why can’t I go faster?” Yet, in 2019, the F.D.A. approved a treatment for some patients with cystic fibrosis, Trikafta, which helps fix the defective protein and directs it to the right place in a patient’s cells. The therapy is projected to extend the lives of patients by decades. As the journalist Sarah Zhang wrote in The Atlantic, “Where they once prepared for death, they now have to prepare for life.” A woman with cystic fibrosis told her, “It’s like the opposite of a terminal diagnosis.” Many patients are now experiencing normal days for the first time, making plans for a future they didn’t think they’d have.
Last fall, I spoke with Sammy Basso, who at twenty-eight was the oldest man known to have progeria. He lived with his parents in Tezze sul Brenta, a small town about an hour’s drive from Venice. He couldn’t remember learning about progeria. It just was, he said, “like an ancestral memory.” As a child, Basso loved science. Like Gordon, he founded an organization to raise money for progeria research; like Kaylee, he spoke eloquently about his condition, in his case on television and with government officials. Basso readily made friends who did not have progeria; a group of them, who called themselves Sammy’s Runners, pushed him in a specialized wheelchair while running marathons. He was also a devout Catholic—Pope Francis gave him a call when he was in high school—and he sometimes wondered, Why is God doing this to me?
During our conversation, Basso was by turns philosophical and self-deprecating. He had a photograph of Sam Berns. “He was a great friend of mine,” Basso said. “I should say, he is a great friend of mine. I believe him to be alive in another dimension.” He told me that he yearned to start a family, even though he knew that his time was limited. He has joked that, because of his slight stature, his doctors put him on a “see food” diet: “When I see food, I eat.” Once, on Halloween, he leaned in to his slight resemblance to E.T. and handed out candy; on another occasion, he donned bright-green sunglasses and greeted visitors outside a U.F.O. museum in Roswell, New Mexico.
In the years since Sam, Kaylee, and Basso were born, scientists have gained the astonishing ability to make changes to a person’s DNA. The best-known method for doing so, CRISPR-Cas9, works like a pair of genetic scissors: a special RNA sequence delivers the Cas9 enzyme, which cuts DNA strands, to a precise location on a gene. When Basso went to college, at the University of Padua, he made CRISPR a focus of his studies, pursuing a degree in molecular biology. In 2019, he co-authored a paper in Nature Medicine that described how the technique could theoretically fix the progeria mutation. He remembered hearing the motto “Together, we will find a cure” and feeling skeptical. But eventually he found himself thinking, Maybe in the very far future we can have a cure.
By the time we spoke, Basso had begun working with David R. Liu, a professor at Harvard and the Broad Institute who has built on CRISPR to develop novel gene-editing techniques. “I’m not doing it for myself,” Basso told me. “It’s for the others.” He had undergone major surgery to repair a failing heart valve. “Progeria has had a lot of time to mess up my body,” he said.
A few days after our conversation, Basso died. He’d collapsed after a night of dancing at a friend’s wedding celebration. Hearing the news, I felt both shock and resignation. I thought of Sam Berns’s advice: never miss a party if you can help it. A letter that Basso had written was read at his funeral. “Death is the most natural thing in life,” the letter said. “If it were not there we would probably not accomplish anything in our lives, because anyway, there is always tomorrow. Death, on the other hand, lets us know that there is not always a tomorrow, that if we want to do something, the right time is now!”
Later, I reached out to Liu, who described Basso as a scientific collaborator and a friend. Their research together was “one of the lasting gifts Sammy gave the world,” Liu said. He spoke about the progress that gene-editing technology has made lately. Another condition caused by an abnormal protein, sickle-cell disease, can now be treated with a recently approved drug. But it does not target the problematic protein or the gene responsible for it—instead, it bolsters a healthy version by disrupting a different gene. A fundamental problem, for Liu, was that many genetic diseases can’t be treated in this way; genetic scissors are simply the wrong tool. “How do you fix a gene with a pair of scissors?” Liu said. “That turned out to be quite a profound question.”
In a landmark 2016 paper, Liu and his colleagues showed that a gene editor his lab had developed could home in on a specific genetic sequence, unravel the DNA, and change one base to another—a C to a T, say, or a G to an A. It was less like a pair of scissors than like a pencil and an eraser. He was invited to give a prestigious lecture at the National Institutes of Health, and before his talk he met with Francis Collins, who had become its director. He knew about Collins’s progeria research, so he mentioned that his method could correct the progeria mutation, at least in human cells in a petri dish. “You have to present that!” Collins told him. Liu looked frantically for a quiet place to revise his lecture. He ended up in the bathroom, laptop open, updating his slides.
Liu began collaborating with Collins and Gordon. (Basso, before he died, often attended their meetings virtually from Italy.) Starting in 2019, the researchers incorporated Liu’s DNA editor into nonpathogenic viruses, injected them into two-week-old mice that had progeria, and found that about thirty per cent of cells in certain organs were successfully edited. The scientists observed a staggering ninety-per-cent reduction in the toxic progerin protein in some tissues, possibly because edited cells replaced unedited cells over time. The hearts, livers, and blood vessels of treated mice appeared strikingly healthy. The data were so promising that they looked unreal, Liu told me.
The mice that didn’t get the gene therapy died after about two hundred days. Those that did lived more than five hundred—the rough equivalent of a human living to retirement age. Liu showed me some videos from the experiment over Zoom. At seven and a half months, the untreated mice looked small and shrivelled, with thin gray coats and curved spines. Next, he pulled up a video of treated mice at eleven months, longer than any of the untreated mice had lived. They were larger, their coats were shinier, and they scurried energetically. “You wouldn’t see them in a pet store and say, ‘Oh, those mice are sick,’ ” Liu said. “It worked better than we could have dreamed.”
Later this year, Liu plans to seek permission from the F.D.A. to move his therapy into clinical trials. Editing the genes of a living person can pose profound risks, however, especially when viruses serve as the delivery vehicle. In 2022, a man with muscular dystrophy received a gene-therapy infusion and died after developing a severe immune reaction. This year, two other recipients of gene therapies, both teen-agers, died of liver failure. “Nobody is under the illusion that you will have anticipated everything,” Liu told me. “You just hope you’ve anticipated most of the important things.” His original progeria base editor was too big to fit inside a single virus, so he had to cut it in half and have it reassembled by what he called “molecular Velcro.” His team has now modified the editor to fit inside one virus, which will hopefully reduce the risks. Gordon named the editor SamPro-1, after her son.
For the first time, it now seems plausible that progeria could be cured. Collins has come to see this possibility as something more. “My commitment, my obsession, with finding a way to cure progeria is of course to help the children who are affected—but also because this could be a new treatment paradigm,” he said. “If we’re successful, it would be the first time we have an in-vivo gene-editing cure of a multisystem disease.” Essentially no treatments have stopped such a complex condition by modifying the DNA inside a living person. “I want progeria to be part of the leading edge of showing what’s possible,” Collins said. He still believes that research into progeria might teach us about aging in general. Even healthy people have been shown to produce the toxic progerin protein in very small quantities; the amount in our bodies increases as we age. Collins told me about an ongoing experiment that modifies the DNA of healthy mice so that they can’t make any progerin. It’s possible that suppressing the protein could help mice, and perhaps one day people, live longer.
Trikafta, the treatment for cystic fibrosis, targets a specific protein and therefore can be used only to treat cystic fibrosis. But a successful gene editor could remedy any number of harmful mutations, solving a fundamental problem in rare-disease research: if there are just a small number of people to pay for novel treatments, companies won’t invest in them. Genetic diseases, in aggregate, afflict more than a quarter of a billion people around the world; every year, they kill millions of children before the age of five. “If something else were killing this many children, there would be an international uproar,” Liu said. “The problem is that all those patients are divided into a thousand subcommunities.” Collins, who directed the N.I.H. until 2021 and left the agency this year, told me, “The dream I have is that you end up with a scalable approach to virtually any genetic disease where you know the DNA mutation. You don’t really even have to understand how a mutation is causing the disease. You just fix it!”
In April, I visited Kaylee at her redbrick home in Perrysburg, Ohio, about fifteen miles south of the Michigan border. My route from the airport passed thick cornfields, lush trees, and expanses of green grass. Kaylee welcomed me into a cozy dining room, where her parents and three adult brothers had gathered for a weekly family dinner. “I hope you like taco bowls,” Marla called out from the stove. Bowls of lettuce, cheese, chicken, and salsa were arranged on a kitchen island.
One of Kaylee’s brothers, Brendan, rose to help her into a seat, then scooped some fruit into a bowl for her. “They’re not always this helpful,” their father, Tim, said, smiling. “In high school, they’d just take her to the mall because they realized that more girls would come talk to them. Kaylee’s a good wingwoman that way.”
“Actually, I just hang out with you to cut the line at airport security,” Brendan offered.
“I put you in my college essay,” another of Kaylee’s brothers, Jacob, said. “Only reason I got in.”
“You owe me!” Kaylee retorted. They reminded me of my relationship with my sister, who was born three months prematurely and given a diagnosis of cerebral palsy. She uses forearm crutches to get around, but for many years she refused to let our family get a disability placard. For her, walking the length of a parking lot was a mark of self-reliance; to me, it seemed like a needless struggle. I feel protective of my sister, but, in part because of her sense of independence, I also try to treat her as I would anyone else. My favorite memories of our childhood are some of the simplest: taking the bus to school; staying up late playing video games; a day we spent on a ranch together, riding horses.
“Who’s the oldest?” I asked, looking around the table.
“Well, T.J.’s twenty-seven, Brendan is twenty-five, and Jacob is twenty-three,” Kaylee said. “But, technically, I’m aging faster than everyone, so that makes me the oldest.”
The next morning, Kaylee picked me up from my hotel for a game of pickleball. Through the windshield of a black van, I saw her slight figure in the driver’s seat. She was wearing sunglasses and peering over the steering wheel. When I climbed into the passenger side, I could see that she was sitting on a kind of booster seat. On her left was a lever that functioned as the brake; on her right, a joystick rotated the vehicle’s wheels. Nearby, a small screen displayed speed and other information. Marla and Iris sat in the back.
“How’s the new medicine been?” I asked as we started driving.
“Pretty good, actually.” There weren’t many side effects, her appetite had improved, and she felt more energetic. Later in the year, her blood would be drawn for a test of its progerin protein levels. “I just hope it gets me to the point where I can benefit from the gene therapy,” she said. “But, in the medical field, everything moves slower than you think. If they say something is one year out, that means three.” Last month, Kaylee celebrated her twenty-second birthday.
We arrived at a park, where a gentle breeze rustled the trees. Brendan and one of Kaylee’s childhood friends, Faith, met us at the courts. Kaylee walked with care, swaying from side to side; she picked up a black racquet and joined Faith on one side of the court, facing off against Brendan and her mother on the other.
After a short rally, Marla knocked the ball into the net. Kaylee turned to me and said, “When you write about this, can you just blame everything on the wind? Like, ‘Four expert players took the court and hurricane winds threw them off their game’?”
Kaylee cautiously bent over to pick up a ball. On the next rally, she accidentally tapped the ball high into the air; Faith ran over and slammed it to the other side. “Assist!” Kaylee yelled. Everyone laughed. A few minutes later, I took Marla’s spot and drove the ball into the net on consecutive points. I could only conclude that the wind was, indeed, a serious impediment.
On a subsequent rally, Kaylee smacked a fierce shot past me, scoring her team a point. She pumped her fist and turned to rile up an imaginary crowd. Then she walked gingerly to the back of the court, took her position, and readied herself for whatever came next. ♦
