Thus, the suppression of canonical Wnt/beta-catenin signaling by nuclear PG recapitulates the phenotype of ARVD by exhibiting fat accumulation in cardiomyocytes, enhanced myocyte apoptosis, ventricular dysfunction, and ventricular arrhythmias in transgenic mice (Garcia-Gras et al., 2006). This evidence concerns the gene CTNNB1 and arrhythmogenic right ventricular cardiomyopathy.