CYBB and endothelial dysfunction: We here provide indirect proof for eNOS uncoupling in the animal models of GTN-induced nitrate tolerance (Knorr et al, 2011; Wenzel et al, 2008) and aircraft noise exposure-mediated cardiovascular damage (Eckrich et al, 2021; Kroller-Schon et al, 2018) by normalization of vascular ROS formation and improvement of endothelial dysfunction by genetic deletion of subunits of the phagocytic NADPH oxidase (NOX-2), namely p47phox or gp91phox, or pharmacological inhibition of the enzyme (Fig. 4).