In the current study, we used a well-established experimental model of DCM-HFrEF in mice [16,22,34,35,36,37,38] to determine if HF progression would be attenuated by the cardiac-specific, transgenic overexpression of catalytically inactive corin, which carries an inactivating mutation in the catalytic triad of the serine protease domain (corin-Tg(i)) (Figure 1a). This evidence concerns the gene CORIN and hydrops fetalis.