Based on current literature, the devised in silico model of ARVC allowed us to draw some important conclusions: (i) simultaneous activation of RhoA-ROCK and canonical Wnt pathways leads to the most effective inhibition of PPARγ expression, the master regulator of adipogenesis; (ii) stability of desmosomes is crucial for the regulation of adipogenesis; and (iii) the overexpression of Wnt5b alone is not sufficient to induce an adipocytic phenotype. The gene discussed is WNT5B; the disease is Arrhythmogenic right ventricular dysplasia.