In animal models, dietary genistein has been demonstrated to be able to decrease the brain oxidative stress induced by stroke in rats, by decreasing the activity of NADPH oxidase enzyme, to reduce superoxide levels, [52] and to decrease ROS and MDA formation, by enhancing antioxidant enzyme activities (SOD and glutathione peroxidase), reversing the mitochondria dysfunction, and suppressing phosphorylation and activation of the NF-κB p65 subunit, and the phosphorylation and degradation of the inhibitor protein of κBα (IκBα) [53]. The gene discussed is SOD1; the disease is stroke disorder.