Other relevant mechanisms related with ACE2 and oxidative stress in the pathogenesis of COVID-19 include the endothelial dysfunction produced as consequence of ROS produced by NAD(P)H oxidase, which reduces the bioavailability of nitric oxide, which in turn results in vasoconstriction, inflammation, redox imbalance, and endothelial dysfunction. The gene discussed is FMO5; the disease is endothelial dysfunction.