Genetic mutations cause cancer. This idea has long driven strategies that aim to lower risk or determine when to look for early signs of disease. Don’t smoke. Minimize alcohol. Get vaccinated against viruses linked to cervical or liver cancer. Lifestyle changes can reduce the chances our cells accumulate DNA mutations that make them grow out of control.

But we might be missing part of the picture. Some people with cancer-related mutations never develop the disease. Others live healthy, have no family history, and suddenly learn they have cancer—and it’s already spread.

To Miriam Merad at Mount Sinai in New York, inflammation is the other half of the puzzle. Cells that acquire mutations and begin to take on cancer-like traits sometimes remain benign, likely because the immune system keeps them in check. By amping up the body’s own surveillance in people with abnormal growths—before they turn malignant—it might be possible to stop tumors from developing in the first place.

The new field, called cancer interception, is gaining steam. Clinical trials for lung cancer are in the works. Cancer vaccines, which train the immune system to destroy abnormal cells, have shown early promise. In one trial, roughly 90 percent of participants with pancreatic abnormalities generated immune cells better able to recognize mutated cells.

Other researchers are taking the idea further. In one study, they gave mice with precancerous pancreatic growths an approved drug to ward off the growths’ transformation into cancer, reshaping the immune landscape and extending survival.

“Yes, those mutations absolutely contribute to dysregulation of the cell that will become cancerous,” said Merad in an interview with Nature .

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