This increase in CaMKII seen in HF could directly promote arrhythmia formation by not only increasing diastolic Ca2+ leak via RyR phosphorylation, but also by promoting increases in the late Na+ current (Wagner et al., 2006), a current that has already been shown to be increased in HF, and incriminated in increased BVR and arrhythmia formation under these conditions (Maltsev et al., 2007). Here, CAMK2G is linked to hydrops fetalis.