Interestingly, human AF patients treated with ACE inhibitors or angiotensin receptor blockers did not show similarly elevated levels of ox-CaMKII as untreated patients (Purohit et al., 2013) consistent with prior observations connecting elevated angiotensin II and aldosterone to the generation of excess ox-CaMKII (Erickson et al., 2008; He et al., 2011). Here, CAMK2G is linked to atrial fibrillation.