While genetic inactivation of PP2Cm leads to global impairment of BCKDH activity and promotes heart failure in ageing or in response to pathological stresses [4, 10], restoring BCKD activity via administration of a highly specific BCKDK inhibitor (BT2) is shown to ameliorate cardiac dysfunction and pathogenic progression of heart failure [11, 12]. The gene discussed is BCKDK; the disease is heart failure.