The locus coding for p16INK4a has been linked to the risk for type 2 diabetes [1] and atherosclerotic vascular disease [2] and bone marrow-specific heterozygous deletion of CDKN2A (including p16INK4a and p19ARF, the murine variant of p14ARF) is required and sufficient to accelerate atherosclerosis formation [10]. This evidence concerns the gene CDKN2A and type 2 diabetes mellitus.