Because SNPs in the Chr9p21 locus have been predicted to influence the expression of CDKN2A/B/ANRIL transcripts [25,26,27,28,29], we can hypothesize that the impairment of p16/Rb and/or p53/p21 pathways may affect the function of cells bearing dysfunctional telomeres (critical telomere shortening), leading to increased senescence and genome instability and, ultimately, promoting the development and progression of atherosclerosis. This evidence concerns the gene TP53 and atherosclerosis.