 In a mouse model harboring knockout of a desmosomal protein, plakoglobin, implicated in arrhythmogenic right ventricular cardiomyopathy, the stabilization of beta-catenin was also enhanced, presumably to compensate for the loss of its plakogloblin homolog.These changes were coordinate with Akt activation and glycogen synthase kinase 3β inhibition, suggesting once again that the abnormal stabilization of beta-catenin may be involved in the development of cardiomyopathy.Further studies employing a double knockout of plakoglobin and beta-catenin showed that the double knockout developed cardiomyopathy, fibrosis and arrhythmias resulting in sudden cardiac death.