KLF15 and familial dilated cardiomyopathy: Indeed, the phosphorylation of p38MAPK (Fig. 2c, k) was increased in the DCM hearts as was the phosphorylation of transforming growth factor-β activating kinase 1 (P-TAK1) (Fig. 2c, l), suggesting that accumulation of cardiac BCAA in the DCM hearts may be triggered by the activation of TAK1, thereby inhibiting KLF15 to down-regulate BCAA catabolism.