The salient features of this study include increased SNRK expression in the atrial chamber compared with ventricles in the mammalian heart, the sensitivity of atrial fibrosis to declining cardiac function, and the identification of SNRK atrial cardiomyocyte-driven repression of TGF-β1 signaling to control cardiac fibrosis, a key cardiac repair process during cardiac regeneration post HF. This evidence concerns the gene SNRK and hydrops fetalis.