In addition to its abundantly studied ventricular consequences, such as in HF and ischemia/reperfusion challenge (Bell et al., 2014), CaMKII has emerged as a key determinant of sinoatrial node dysfunction (as well as a central regulator of physiological sinoatrial node responses) (Wu and Anderson, 2014; Yaniv and Maltsev, 2014). Here, CAMK2G is linked to hydrops fetalis.