Furthermore, Ang II‐induced hypertension and vascular dysfunction are associated with increased vascular reactive oxidative stress (ROS) production.34 Although the exact cellular sources of ROS have not been defined, macrophages are believed to be the main source of ROS in the vessel.35 Inhibition of platelet activation effectively reduced the vascular levels of NADPH oxidase subunits such as NOX‐1, 2, and 4, and was associated with reduced infiltration of macrophages in the aorta in response to Ang II. The gene discussed is FMO5; the disease is hypertensive disorder.