Finally, AT1R receptor activation in arterial smooth muscle cells inactivates nitric oxide by interacting with radical producing systems such as the NADPH oxidase (thereby further aggravating the eNOS dysfunction-related impairment of NO bioavailability), and is thought to represent a key event in promoting [26,27] premature vascular aging and atherosclerosis [28]. The gene discussed is FMO5; the disease is atherosclerosis.