65 DNA demethylation causing overexpression of the KLF4, KLF5 and OPN genes leads to the increased mitotic activity of smooth muscle cells in coronary vasculature.66 Hyperacetylation of histone proteins H3K9 and H3K27 has been implicated in stabilizing atherosclerotic plaques.67 Moreover, alteration in histone proteins associated with oxidized low-density lipoprotein-mediated inflammatory response is crucial in the pathogenesis of coronary artery disease (CAD) in T2DM. The gene discussed is KLF4; the disease is coronary artery disorder.