PPARG and arrhythmogenic right ventricular cardiomyopathy: This helps explain the phenotype of ARVC in humans and makes it possible to link genetic desmosomal abnormalities to the presence of fat in the right ventricle of ARVC patients, due to dysfunction of PPARγ and α. Other earlier studies have shown that disruption of Wnt/β-catenin signaling causes transdifferentiation of myoblasts into adipocytes in vitro [33] and leads to activation of PPARγ.