In this study, the authors utilized BT2 (3,6-dichlorobenzo(b)thiopene-2-carboxylic acid), a BCKDK inhibitor, to promote BCKDH-mediated BCAA catabolism in myocardial infarction (MI)-operated mice, suggesting that restoring BCAA catabolism could ameliorate cardiomyopathy in humans. Here, BCKDK is linked to myocardial infarction.