At the cellular level, major ROS sources—including the mitochondrial respiratory chain, NADPH oxidase, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS)—contribute to endothelial dysfunction, vascular smooth muscle cell proliferation, and the oxidation of low-density lipoproteins (LDL). This evidence concerns the gene FMO5 and endothelial dysfunction.