CDKN2A and atherosclerosis: Cellular senescence, defined as a permanent cessation of the cell cycle, is associated with the activation of the p16INK4a/Rb and p19ARF/p53 pathways, as well as metabolic dysregulation and the emergence of pro‐inflammatory phenotypes.[10] Advanced atherosclerotic plaques contain cells exhibiting senescence markers, which may serve as a significant source of inflammatory cytokines.[4] Senescent foam cells are detrimental throughout all stages of atherosclerosis, although their specific roles remain poorly understood.