Therefore, combating ROS-induced cellular damage and preventing MPTP opening by enhancing GSH/GSSG (the largest capacity thiol buffer in the cell, the reduction of which is one of the major mechanisms that prompt the opening of MPTP in diabetes [57]) and inhibiting xanthine oxidase could be the fundamental mechanism explaining why NAC and ALP attenuate the augmented myocardial post-ischemic injury in diabetic rats and ameliorate post-hypoxic cardiomyocyte injury under high glucose stimulation. The gene discussed is XDH; the disease is diabetes mellitus.