Based on their high sequence similarity, PG and β-catenin compete for the binding to TCF/LEF, but they have opposite effects in the regulation of the adipogenic program: the effect on gene program elicited by PG was described as mechanism responsible for ARVC, and for the lineage conversion from cardiac myocytes to adipocyte-like cells, while β-catenin binding to TCF/LEF suppresses adipogenesis. Here, HNF4A is linked to arrhythmogenic right ventricular cardiomyopathy.