Our data also support an observation in a randomized control trial and other rat models of DCM in which ALA administration prevented an increase in heart mitochondrial ROS production and effectively enhanced SOD activity and GSH content of myocardial mitochondria as well as decreased collagen deposition and TGF-β1 and mitochondria-dependent cardiac apoptosis (Midaoui et al., 2003; Li et al., 2009; Lee J. E. et al., 2012; Hegazy et al., 2013). The gene discussed is SOD1; the disease is familial dilated cardiomyopathy.