The cardiovascular benefits of SGLT2 inhibitors in heart failure, thus, could also be achieved in glucose-independent manner by acting as an antioxidant restoring oxidant-antioxidant balance through several mechanisms including inhibition of eNOS uncoupling, downregulation of NADPH oxidase expression, and attenuation of overexpressed superoxide dismutase25. The gene discussed is FMO5; the disease is heart failure.