For example, Menu P et al. (83) found no differences in the progression of atherosclerosis, plaque infiltration, or plaque stability in ApoE-deficient mice that lack either Nlrp3, Asc, or caspase-1 compared with wildtype mice, presenting conflicting evidence that atherosclerosis develops independently of NLRP3 inflammasome in ApoE–/– mice. This evidence concerns the gene CASP1 and atherosclerosis.