Therefore, SERCA2a and PLN are expected as a target for novel therapy of HF for a few decades, indeed, it was reported that the normalization of SERCA2a function and the PLN inhibition increased contractility with correction of Ca2+ homeostasis in a large number of studies in isolated cardiomyocyte and animal models of HF [17–19]. The gene discussed is PLN; the disease is hydrops fetalis.