In vivo experiments showed that PP2Cm-overexpressing ADSCs had a much higher retention rate and better cardioprotective effects against post-MI cardiac dysfunction and remodeling, whereas ADSCs with BCKDK overexpression were intolerant of the post-myocardial infarction milieu and completely lost their cardioreparative potential. The gene discussed is BCKDK; the disease is myocardial infarction.