Overexpression and activation of CaMKII leads to increased diastoliccalcium leak from the sarcoplasmic reticulum and increased cytosolic calcium,leading to contractile dysfunction and proarrhythmic effects [124, 125].Furthermore, NHE1 mediates sodium influx in the cardiomyocyte and its activity isincreased in the failing heart, contributing to the cellular sodium overloadwhich is characteristic of HF [118]. This evidence concerns the gene CAMK2G and hydrops fetalis.