Senescence is thought to be an important regulator of the atherosclerosis process,[4] particularly associated with lipid metabolism disorder.[20] Previous studies have indicated that senescent cells exhibit an increased capacity for lipid uptake,[21] and our research also demonstrated an upregulation of CD36, a principal lipid receptor in macrophages, in immune cells derived from diabetic Apoe−/− mice (Figure 2F). This evidence concerns the gene CD36 and Disorder of lipid metabolism.