Quite strong evidence supports a role for vascular smooth muscle Nox1 in AngII-induced hypertension, involving changes in vascular remodeling.10,11 The cell-specific role of Nox2 is unclear, but this a pertinent question because Nox2 is expressed in endothelial cells, cardiomyocytes, fibroblasts, certain vascular smooth muscle cells, and inflammatory/immune cells.6 Nox2 is involved in the genesis of endothelial dysfunction in diverse models,6,7 and previous studies from our laboratory21 and others32 found that endothelium-targeted overexpression of Nox2 enhanced AngII-induced hypertension. This evidence concerns the gene AGT and endothelial dysfunction.