P‐selectin deficiency has been associated with a reduction in inflammation and in the progression of atherosclerosis in ApoE‐null mice.30 In addition, P‐selectin inactivation limits plaque macrophage content and neointima formation after endothelial injury in the carotids of ApoE‐null mice.31 Altogether, these data further support the essential role of inflammation, leukocyte adhesion, and macrophages in the initiation of the atherosclerotic process in dyslipidemic mice. This evidence concerns the gene APOE and atherosclerosis.