In support of a relevant causative contribution of oxidative stress to the pathogenesis of DCM, reduction of ROS levels by the administration of antioxidants, such as dehydroepiandrosterone (DHEA) [33] to rodent models, as well as the ectopic overexpression of catalase [37] or superoxide dismutase [35], have been shown to reduce cardiac fibrosis and to improve cardiac contractile function. The gene discussed is CAT; the disease is familial dilated cardiomyopathy.