Nox1, at least preclinically plays only a minor role in both comorbidities10–12; knocking out Nox2 even increases infections and mortality in diabetes and is thus not a viable target10; Nox3 seems to be involved in pulmonary hypertension13; Nox4 is, surprisingly, rather atheroprotective14,15 and downregulated in abdominal aortic aneurysm6; Nox5 appear to stand out in atherosclerosis, at least by the clinical correlation of its expression levels in endothelial cells, both in early stages of coronary artery disease and aortic aneurysm6,7,16. This evidence concerns the gene CYBB and atherosclerosis.