In AF, increased oxidative stress could have resulted in the upregulation of pro-oxidant enzymes, including NADPH oxidase, or the downregulation of circulating antioxidant systems such as superoxide dismutase (SOD) or glutathione peroxidase 3 (GPx3), which led to an increased concentration of reactive oxidant species. The gene discussed is SOD1; the disease is atrial fibrillation.