We found that a significant gain in [Na+]i (~ 3–4 mM), which is what happens in HF (Despa et al., 2002), induces an increase in Ca2+ and consequent Ca2+-dependent CaMKII activation, which in turn enhances Na+ and Ca2+ signals, leading to a pro-arrhythmic condition. This evidence concerns the gene CAMK2G and hydrops fetalis.