When I met “Sean” my freshman year at Duke, we didn’t like each other much. He found me prickly, and I found him unfunny. Despite this, a shared need for help on statistics homework forced us into a grudging peace.

Eight years later, I’m a graduate student studying genetics, and Sean is getting his own graduate degree. I find time to call him every few weeks, just to see if he’s dating anyone yet.

When I met Sean, he was already dying. At twelve years old, Sean was diagnosed with idiopathic chronic recurrent pancreatitis. Two to three times a year, his pancreas starts digesting itself, sending him to the emergency room for weeks. Each attack progresses the disease, making the next attack more violent and more likely to kill. Idiopathic means there is no known cause, and therefore no cure.

In 2020, an attack hospitalized Sean for a month. The pain was so bad that Sean broke his façade and begged a nurse to kill him. He told me a few months ago, as part of an elaborate joke.

I still don’t think he’s funny.

Recently, a doctor asked Sean to undergo genetic testing. He thought nothing of it. But about a month ago, the results showed two mutations in Sean’s DNA that decrease levels of the vitally important protein SPINK1. It turns out that SPINK1 is a preventative protein. It blocks another enzyme named trypsin, since too much trypsin can cause autodigestion of the pancreas. 

Suddenly, we had a cause. Idiopathic chronic recurrent pancreatitis became chronic recurrent pancreatitis.

Given the cause, we found that researchers at the Wyss Institute for Biologically Inspired Engineering — a research institute at Harvard University working on diagnostics and therapeutics — developed a preliminary drug just this February that provides artificial SPINK1 to the body. It prevents pancreatitis in experiments in mouse models, and is progressing towards human clinical trials. For the first time in fifteen years, Sean had a way forward.

As a geneticist, I work on improving disease treatment by tailoring medicine to our genetics. Specifically, I study how genes regulate each other to cause disease. My roommate actually studies rare diseases like Sean’s. 

To then see genetics directly change Sean’s life felt almost … sacred. After all, scientists are motivated by real-world impact. We put up with low pay and years of extra schooling, all hoping our research will one day change lives. For it to happen for Sean … I think I’ve never felt quite that happy, in quite that way, before.

For the record, I told Sean to get tested for years. He never listens to me.

But now to my point. The Wyss Institute is backed by Harvard — which recently lost $3.2 billion dollars in federal research grants. These funding freezes could delay or cancel clinical trials that could save Sean’s life. And this situation isn’t unique — basic science is under threat across America. Congress is debating a budget that would cut $18 billion from the National Institutes of Health (NIH), which would shrink the country’s primary funding source for drug research by about 40%. 

We don’t know what we’ll lose with these cuts. A month ago, I had no idea Sean’s disease was genetic. Today, it’s a certainty. Science moves just as dramatically. Thirty-five years ago, we didn’t even know the sequence of the human genome. But just this past May, scientists successfully treated a baby with a life-threatening genetic disorder, one similar to Sean’s, by changing a specific mutation in his genome. In another thirty-five years, it’s impossible to know what treatments will be available to us — or what might be lost without proper funding.

Sean’s favorite joke is that if I don’t hurry up and get married, he’ll die before my wedding. He’s not wrong, even if he’s still not funny. People like Sean can’t wait for the next election cycle. Durham and Wake County alone have already lost a combined $754 million and around 3200 jobs. At Duke alone, projected future losses range between 500 and 750 million dollars — money which pays student salaries, keeps the lights on and maintains necessary lab equipment. Science is already suffering.

Some costs can’t be measured in dollars. In response to the cuts, many graduate programs are cutting or stopping admissions. The Duke University School of Medicine, for example, will reduce its class size from 130 PhD students to a target size of 100. At the same time, alternate paths for funding like scientific fellowships have dried up. The next cycle of applicants faces steeper competition, with less money, for fewer positions and a less certain future. Meanwhile, the potential cuts have also limited our country’s ability to recruit talent from abroad. If we’re not careful, we stand to push away an entire generation of scientific talent.

How can we help Sean, and everyone else who relies on science? We can remind ourselves, and those around us, that scientific research finds cures that transform lives. We can remind ourselves that science is fragile, and often, the first thing to go is research for rare diseases like idiopathic chronic recurrent pancreatitis.

More importantly, we can remind our representatives. Call them today! Ask them if they’ve heard of idiopathic chronic recurrent pancreatitis, or other disorders that impact your loved ones. Tell them that science matters, that your loved ones matter, and that you support funding scientific research.

I’ll end by saying that Duke is where I was trained. Professors like Owen Astrachan, Leslie Saper and Jayce Getz instilled (sometimes painfully) a foundation in math and computer science that I have relied on ever since. I am a more capable scientist today because my professors — and a small army of graduate teaching assistants — cared about my education. And while this piece is about science funding, I could not have written it without humanities professors and graduate students like Cathy Schuman and Claire Ravenscroft, who shaped me as a writer, thinker and person. 

Duke is also where I decided to study biology. I study genetics now in large part because Alexander Hartemink’s lectures made biology feel exciting and knowable, and inspired me to work with him. I can explain Sean’s genetics to you today because six years ago, a kind man thought it was important to keep teaching an undergrad even though he kept falling asleep in lab meetings.

To these people and others, I am grateful. I am so lucky to be part of Duke’s rich history of math, science and the humanities. But these same professors face the most uncertain future for education and research in recent memory. Please help them keep that history alive for generations to come.

Finally, Duke is where I met Sean. We fought over FIFA, ate McDonald’s at 3 a.m. and were happy. He was dying then, and luckily still is. He does not share easily, but I asked him to anyway, because it was important.

Thanks, Sean. Get some new jokes, please.

Albert Xue, Trinity ’20, is a graduate student at UCLA Bioinformatics.