Clinical studies have reviewed the possible impact of oxidative stress in the pathophysiology of depression [271,272,273,274], focusing on ROS iper-production or on the activation of enzymes relevant in pro/antioxidant processes [e.g., NOX, XO, superoxide dismutase (SOD) and catalase (CAT)] [274], and experimental models have established that the enhanced ROS production favors depression-like phenotype [275]. The gene discussed is SOD1; the disease is depressive disorder.