Many experimental evidences suggest that a RhoA-ROCK pathway may play a critical role in ARVC pathogenesis, and recently, Dorn and co-workers have proposed the first mechanism by which mechanical signals through cell-cell contacts translates to a myocytic-to-adipocytic switch in ARVC, suggesting that cardiomyocytes identity is controlled by various pathways converging to RhoA/MRTF/SRF signaling. This evidence concerns the gene RHOA and Arrhythmogenic right ventricular dysplasia.