In the pathogenesis of atherosclerosis, multiple stimuli, such as oxidized low-density lipoproteins (LDLs), high glucose level, uric acid, and homocysteine, damage the integrity of the vascular endothelium, cause vessel leakage, increase leukocyte adhesion to the clammy endothelium, induce VSCM contraction, lead to endothelial nitric oxide synthase (eNOS) uncoupling, and decrease NO production [51]. The gene discussed is NOS3; the disease is atherosclerosis.