NADPH oxidase, specifically NOX2, the isoform expressed in cerebral endothelial cells, perivascular macrophages, microglia, and astrocytes, is likely the main source of increased cerebral superoxide anion in Ang II-induced hypertension in mice [5,10,24].Moreover, NOX2−/− mice are protected from the Ang II-induced NVC alteration [5], further confirming the role of oxidative stress on cerebrovascular dysfunctions. Here, FMO5 is linked to hypertensive disorder.