Recent studies on human arteries from patients with coronary artery disease (CAD) [58], and experimentally induced hypertension [40], diabetes and atherosclerosis [59] in animal model systems suggest that Nox1, 2 and 5 all promote endothelial dysfunction, inflammation, and apoptosis within the vessel wall [1], whereas Nox4 is by contrast vasoprotective via increasing NO bioavailability and suppressing apoptotic pathways (Figure 2). The gene discussed is NOX1; the disease is atherosclerosis.