Mice globally deficient in p47phox, a subunit required for both Nox1 and Nox2 function, display a reduced hypertensive response to AngII,9 as do global Nox1 knockout (KO) mice,10 whereas vascular smooth muscle–targeted Nox1 transgenic mice develop exaggerated AngII-induced hypertension.11 The role of Nox2 is less clear. Here, NOX1 is linked to hypertensive disorder.