Importantly, these researchers showed that inhibition of mTOR by rapamycin or pharmacological inhibition of branched chain keto acid dehydrogenase kinase, a down-regulator of myocardial BCAA catabolism, significantly improves cardiac BCAA catabolism, reduces amounts of myocardial BCAA, and ameliorates post-MI cardiac dysfunction and remodelling. The gene discussed is BCKDK; the disease is myocardial infarction.