The increased SR Ca2+ load could be explained with increased SERCA Ca2+ reuptake modulated by increased PLB phosphorylation via CaMKII at Thr17 [11,18] or decreased sarcolipin [17,64] in atria with HF, even though the SERCA2a and PLB expressions were unaltered or decreased [11, 17,18,64]. The gene discussed is SLN; the disease is hydrops fetalis.