At later stages, disturbed Ca2+ cycling, as evidenced by CaMKIIδ activation and protein kinase B/AKT inactivation, are visible in the VO model and probably contribute to the HF phenotype2, suggesting that maintenance of AKT and/or antagonizing CaMKII signalings might be promising therapeutics to avert maladaptive remodeling in response to VO. This evidence concerns the gene AKT1 and hydrops fetalis.