Our study follows the groove of the identification of the physiological implications of CaMKs in the cardiovascular system.1–3 Some authors have investigated the effects of CaMKIV in the heart by overexpressing it in cardiomyocytes, leading to cardiac hypertrophy.46 This notion was challenged by a more recent study showing that mice null for CaMK4 still developed LVH.4 Our data reconcile these opposing views by suggesting that dysfunctional CaMKIV, albeit not expressed in the heart, might partake in cardiac organ damage in the context of the hypertensive state. The gene discussed is CAMK4; the disease is cardiac hypertrophy.