Inhibition of CaMKII or elimination of CaMKII-dependent RyR2-phosphorylation has proven antiarrhythmic in mouse models of AF and has shown beneficial effects in atrial cardiomyocytes from cAF patients (Chelu et al., 2009; Li et al., 2012; Voigt et al., 2012). The gene discussed is CAMK2G; the disease is atrial fibrillation.