Genetic ablation of CaMKII-dependent RyR2 phosphorylation in the S2814A mouse provides protection from pacing-induced arrhythmias after pressure-overload, slows the development of contractile dysfunction, and reduces ventricular remodeling and cellular SCR (van Oort et al., 2010; Respress et al., 2012). The gene discussed is RYR2; the disease is Arrhythmia.