Furthermore, it has been reported that cholesterol crystal, a hallmark of atherosclerotic lesions (80), activates NLRP3 inflammasome in a process involving lysosomal rupture, and reconstitution with NLRP3-, ASC-, or IL-1α/β–deficient bone marrow in low-density lipoprotein receptor (LDLR)–deficient mice shows reduced early atherosclerosis, suggesting the link between NLRP3 inflammasome and pathogenesis of atherosclerosis (9). The gene discussed is IL1A; the disease is atherosclerosis.