To evaluate this hypothesis, we took a gain-of-function approach and measured the effects of VDAC2 agonist efsevin in murine tissue from failing hearts: in line with the HF phenotype induced by VDAC2-KO, efsevin enhanced contractile force in failing myocardium from a murine pressure-overload model establishing VDAC2 as a promising target for HF. The gene discussed is VDAC2; the disease is hydrops fetalis.