Noting that many of the central coordinators significantly regulated by PPP1R3A knockdown were metabolic genes (e.g. GLUT4, PFK, multiple subunits of NADH ubiquinone oxidoreductase and COQ10, Fig. 4b) and that prior work has implicated PPP1R3A in striated muscle glycogen metabolism, we hypothesized that PPP1R3A’s role in the development of HF was related to the metabolic switch from respiratory to glycolytic glucose metabolism observed in failing myocardium. The gene discussed is PPP1R3A; the disease is hydrops fetalis.