We have also recently reported the contribution of MAO-related vascular oxidative stress to the endothelial dysfunction in human mammary arteries harvested from overweight patients with HF with mildly reduced ejection fraction undergoing revascularization procedures; in this pilot study, ex vivo incubation with empagliflozin alleviated endothelial dysfunction, mitigated oxidative stress, and decreased vascular expression of both MAO-A and MAO-B [23]. The gene discussed is MAOA; the disease is endothelial dysfunction.