These studies suggest important concepts that require more investigation as it relates to SNRK’s role in HF, which include: (1) SNRK-mediated cell-cell communication in the heart; (2) pharmacological activation of SNRK selectively in CMs to suppress inflammation and metabolic dysregulation; and (3) SNRK activation in CMs to promote cardiac output via mitochondrial or other mechanisms. This evidence concerns the gene SNRK and hydrops fetalis.