The results, published this August, are provocative: Despite no change in cholesterol levels, there was a demonstrable reduction in heart attacks, stroke and cardiovascular death, particularly at higher doses of the drug. But what caught my attention was a separate analysis that asked a seemingly unrelated question: Might the drug also reduce the risk of cancer? In a paper published in The Lancet, Ridker and his colleagues found that drug-treated patients had a drop in all cancer mortality. More striking still was a stark decrease in the incidence of and deaths from lung cancer. Some element of inflammation that drives plaque formation in coronary disease is also driving cancer progression. It’s a study that needs careful replication; the analysis was designed to suggest a hypothesis, not to prove it. There are questions about drug pricing and the risks of infections and low blood counts. But if the benefit holds up in future trials, interleukin-1-beta inhibition could eventually rank among the most effective prevention strategies in the recent history of cancer.

Inflammation at the nexus between cancer and heart disease? But of course, some of you must be thinking, with an exasperated nod. You’ve had your third serving of blueberries; you’ve drunk your green tea. Wasn’t it obvious all the while?

It isn’t so simple. An avalanche of studies has implicated inflammation as a central player in many diseases — but there are inconsistencies. Consider an inflammatory illness like lupus: The risk of most cancers (except some virally related cancers and lymphomas) in lupus patients is only marginally higher. Rheumatoid arthritis increases the risk of lymphomas — but oddly lowers the risk of breast cancer. Tuberculosis, an inflammation-inducing disease, appears to promote lung-cancer risk, but in an animal study, eczema, weirdly, reduces the risk of skin cancer. Meanwhile, an alternative-medicine industry daily peddles “anti-inflammatory” diets — but which of these reduce inflammation, or what types of inflammation are affected, remains far from known.

“Inflammation,” in short, is a concept in flux — “a wastebasket word,” as Padmanee Sharma, an immuno-oncologist at M.D. Anderson Cancer Center, told me. There isn’t one inflammation: Lupus, tuberculosis and influenza all cause “inflammation,” but each might provoke different or overlapping wings of immune responses. I asked James Allison, who pioneered cancer immunotherapy, to define “inflammation,” and he paused, considering the definition. “It’s a response to injury, mediated by immunological cells. But there are dozens of cell types communicating through even further dozens of signals.”

We might imagine inflammation, then, as a fuse box that you chance upon in a new house. You are looking for the switch that turns the light on in the living room, or one that turns the alarm off (just as we’re hoping to throw the switch that disables cancer growth or plaque formation). But the circuitry baffles you. Some knobs are marked in crimson: Do Not Touch. Some carry no labels. Some do, but the writing is in a foreign language.

“Inflammation, an umbrella term, is now being broken up into many different categories,” Sharma told me. Is it chronic or acute? Is there a “right” kind of inflammation that protects us from infections and a “wrong” kind that precipitates disease? Is it mediated “adaptive” immunity — the type of immunity involving B and T cells that adapts to infections? Or “innate” immunity, the more ancient phalanx of immune responses that is preprogrammed to fight certain pathogens?