Consistent with this postulation, a recent study of mice dually lacking RGS2 and RGS5 (Rgs2/5 dbKO) reported a set of phenotypes that are hallmarks of DCM, including left ventricular (LV) dilatation and contractile dysfunction, accompanied by higher rates of excitation-contraction coupling abnormalities in LV cardiomyocytes, with increased arrhythmia burden and sudden death in Rgs2/5 dbKO mice (46). The gene discussed is RGS2; the disease is cardiac arrhythmia.