As reported [27], chronic IL-1 blockade increases the risk for fatal infections and sepsis, suggesting that selective targeting of the NLRP3 inflammasome may potentially be a safer and more efficacious therapeutic strategy because it would block production of the central inflammatory mechanisms that contribute to inflammatory pathology while at the same time keeping nontargeted inflammasomes available to produce IL-1β to cope with infections. This evidence concerns the gene NLRP3 and infection.