You are what you eat, but what happens to those calories after you eat may depend more on your genes than you think.

Scientists have long suspected that how our bodies deal with calories is somewhat determined by our genetic makeup. Now they’ve zoomed in on one gene—FNIP1—that plays an outsize role in how we burn energy and what our risks of obesity, diabetes, heart disease and kidney disease are. Around one in 7,000 people carries a broken copy of this gene that almost acts like a GLP-1 drug—the body burns fuel more efficiently, and the risk of disease lowers.

To find the gene, scientists sequenced the coding DNA of more than a million people across three continents to scour for mutations that influence how the body stores and uses fat. FNIP1 stood out.

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Paired with a protein called folliculin, FNIP1 slows down cells’ calorie-burning machinery to conserve extra energy when food is plentiful. That’s proved useful over most of human history, enabling us to survive through times when food has been scarce. But if you nix the gene, the opposite happens: the body burns through energy faster and uses up fat instead of storing it, says Viktoria Gusarova, a researcher at Regeneron Pharmaceuticals and a co-author of a study detailing the work.

We inherit two copies of a gene, one from each parent. As noted, around one in 7,000 people will inherit a broken copy of FNIP1. In the study, around 150 people had this mutation. They also had lower blood lipids, less liver fat, lower blood sugar, proportionally more muscle and roughly 60 percent lower odds of cardiometabolic diseases, such as obesity and diabetes.

“These individuals consume, store and utilize energy more than individuals without those mutations, and that's the protective factor,” explains Luca Lotta, a geneticist at Regeneron Pharmaceuticals and the study’s co-senior author.

The researchers went further, looking at liver cells in the lab to see if silencing FNIP1 could turn on fat-burning genes. And in mice fed a fatty, sugary diet, shutting the pathway down in the liver curbed weight gain, cleared out fat and improved insulin sensitivity. Over 30 weeks, it also prevented the fibrosis and liver damage the diet would otherwise cause. The research was published in Nature.

The mutation is so rare, Lotta says, because evolution can’t keep up with our changing world. “Nowadays, we are living in a very calorie-rich environment and historically there’s no precedent for this”, Lotta says. “These incredibly rare mutations, which might have been unfavorable for many millennia, are now favorable to the body.”

The team hopes the mutation could help lead to drugs that mimic its effects.

“Individuals with loss of function genetic variants can naturally mimic effects of pharmacologic inhibitors and such studies have led to important therapeutic advances in other diseases,” says Svati Shah, the director of the Center for Precision Health at Duke University who was not involved in the study. Whether deliberately switching off FNIP1 in humans is safe, however, is unclear.

Notably, people who inherit two broken copies of FNIP1 instead of just one are prone to heart disease and immune deficiency. “If you were to therapeutically inhibit the gene everywhere in the body at 100 percent, that could have a negative impact on health,” says Lotta. He suspects that targeting the gene in the liver alone might mitigate the risks. “Any therapy is many years away, though,” he says.