A widely used model of atherosclerosis (Apolipoprotein E double knockout mice, ApoE-KO) showed that early atherosclerotic plaques were enriched with M2-like macrophages, which promoted the proliferation of smooth muscle cells in vitro, whereas, in elderly mice, a transition from an M2 to M1 phenotype was observed, which is due to the repolarization of macrophages in the lesion. This evidence concerns the gene APOE and atherosclerosis.