Consistent with chronic CaMKII activation being a causal factor in the development of the disturbed Ca2+ phenotype, cardiomyocytes isolated from 11–13 week old CaMKIIδC overexpressing transgenic mice showed signs and symptoms of HF and were characterized by highly elevated diastolic [Ca2+] and slowed CaT kinetics in both subcellular compartments [25]. This evidence concerns the gene CAMK2G and hydrops fetalis.