However, chronic IL-1-blockade increases risk for fatal infections and sepsis, suggesting that upstream targeting of the NLRP3 inflammasome may potentially be a safer and more efficacious therapeutic strategy as it would block production of the central inflammatory mechanisms that contribute to the pathology while at the same time keeping non-targeted inflammasomes available to produce IL-1β to cope with infections (Ridker et al, 2017). The gene discussed is IL1B; the disease is infection.