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. The gene discussed is MEFV; the disease is cryopyrin-associated periodic syndrome.