Endothelial damage in the early stage of atherosclerosis leads to the oxidation of low-density lipoprotein cholesterol (LDL) in the subendothelial cavity to form oxidized LDL (ox-LDL) [7, 70], which can inhibit the activity of NOS in endothelial cells and accelerate the degradation of NO, thereby reducing biologically active NO and the bioavailability of NO, eventually causing endothelium-dependent vasodilation abnormalities. This evidence concerns the gene NOS2 and atherosclerosis.