The ability to selectively target an aberrant inflammasome, for example the Pyrin inflammasome in patients with FMF or the NLRP3 inflammasome in patients with CAPS, while leaving the others free to respond to infections and other insults, presents an attractive alternative to a total blockade of IL-1β signaling or inhibiting a shared downstream effector molecule. This evidence concerns the gene NLRP3 and infection.