These results suggest that reducing around half of the EPRS1 protein expression in CMs does not cause any cardiac dysfunction or cardioprotective effects in mouse hearts at baseline and under pressure overload conditions, supporting the observation that a low-dose halofuginone-mediated inhibition of prolyl-tRNA synthetase activity does not cause severe cardiotoxicity in the pressure overload-induced HF model [7]. The gene discussed is EPRS1; the disease is hydrops fetalis.