Wild type mice models are resistant to atherosclerosis development due to the low level of low-density lipoprotein (LDL), therefore, apolipoprotein E-deficient (ApoE−/−) mice and LDL receptor knock-out mice which display poor lipoprotein clearance with subsequent accumulation of cholesterol, that promote the development of atherosclerotic plaques, are the most common mice models to study the pathophysiology of atherosclerosis. This evidence concerns the gene APOE and atherosclerosis.