On the other hand, the overexpression of Nox1 enhances Ang II‐induced O2− formation, VSMC hypertrophy, and hypertension in transgenic mice.99 Furthermore, in cytosolic NAD(P)H p47phox subunit‐deficient mice, the endothelial dysfunction, O2− production, and Ang II‐induced hypertensive response were blunted.63 Moreover, NAD(P)H oxidase was associated with raised O2− production in the arterial tissue of SHR.92 The gene discussed is FMO5; the disease is hypertensive disorder.