Minhas et al. have supported the idea that XOR is the primary source of ROS generation in the failing heart and that its upregulation contributes to maladaptive cardiac hypertrophy, directly participating in the progression of LV failure, since chronic XO inhibition with oxypurinol reverses left ventricular (LV) remodeling and improves LV function following experimental myocardial infarction in rats [38]. The gene discussed is XDH; the disease is myocardial infarction.