In both WT and PP2Cm KO hearts, silencing of KDM4E markedly improved the therapeutic potential of ADSCs on cardiac dysfunction and remodeling after MI to the same degree (supplementary Fig. 6d, e and Fig. 4g–j), demonstrating in vivo that KDM4E silencing overcomes the adverse effects on the adaptation and cardioprotection mediated by the high BCAA levels in the post-infarction heart. Here, KDM4E is linked to infarction.