Bacterial infections that cause sepsis are a problem of colossal proportions. In the United States alone, 18% of people admitted to hospital in 2000 as a result of this form of systemic inflammation died1, and mortality associated with sepsis is rising. Studies of animal models have revealed that the molecular process underlying sepsis involves the proteolytic enzyme caspase-1. On page 117 of this issue, Kayagaki and colleagues2 provide a crucial reappraisal of this conclusion. They show that mice lacking the gene that encodes caspase-1 also carry a mutation in a less-studied neighbouring caspase gene that is, in fact, responsible for some of the effects attributed to caspase-1 — including sensitivity to sepsis in animal models.
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