Hyperhomocysteinemia increases oxidative stress and is closely related to accumulation of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide (NO) synthase (NOS) inhibitor that inhibits the activity of endothelial NOS (eNOS) and inducible NOS (iNOS) which play crucial role in cardiovascular regulation [43–45]. The gene discussed is NOS3; the disease is hyperhomocysteinemia.