Based on studies with atherosclerosis-prone apolipoprotein E (apoE) or LDL receptor (Ldlr)-deficient mice fed a high fat/high cholesterol diet, it has been shown that deficiency of Nlrp3, caspase-1, Asc, Il1b or Il18, as well as blockade of IL-18, results in a reduction in number and size of atherosclerotic lesions and a higher stability of atherosclerotic plaques [19,68,69,70,71,73]. This evidence concerns the gene APOE and atherosclerosis.