The mechanism by which mutated TET2 promotes the development of cardiovascular disease has not yet been fully understood; however, used as model in atherosclerosis-prone, low-density lipoprotein receptor-deficient (Ldlr−/−) mice, it has been shown that TET2 mutations favor the recruitment of macrophages in the endothelium, thus promoting the inflammatory state, which is believed to cause the rapid development of atherosclerotic plaques [132]. This evidence concerns the gene TET2 and atherosclerosis.