H3K9me2-mediated regulation of inflammation-induced genes in VSMCs might also explain the accelerated neointima formation following vascular injury previously detected in diabetic rats when H3K9me2 levels were reduced by overexpression of KDM3A, a H3K9me2-specific demethylase.62,63 VSMCs from diabetic patients also display reduced levels of H3K9me2 compared with nondiabetic controls, and KDM3A is induced by high insulin levels.62,64 Therefore, dysregulation of H3K9me2 might contribute to diabetes-associated vascular complications. This evidence concerns the gene MBD2 and diabetes mellitus.