CDKN2A and atherosclerosis: 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.