TBPL2 and ischemia: Interestingly, despite the fact that the deletion of TBP-2 could facilitate mitochondrial function in reducing ischemia-reperfusion damage, it has been verified that TBP-2 enhances the destruction of the myocardium, generated by ischemia-reperfusion via weakening anaerobic metabolism (e.g., anaerobic glycolysis), which enlarges the infarct size after a reversible coronary ligation [2].