RYR2 and hydrops fetalis: Extensive studies demonstrate that activated CaMKIIδ is critically involved in phosphorylation of RyR2 at the site of Ser2815, resulting in sensitized RyR2 channels and profoundly increased diastolic SR Ca2+ leak that in turn promotes triggered activities and arrhythmia initiation in pathologically altered ventricles in HF [2, 6, 51, 56, 87, 91, 111, 127, 150, 155, 156, 158].