Our data showing reduced levels of TRAF2 (Figure 5A,B), and upregulation of RELB, a positive regulator of non-canonical NFĸB signaling (Figure 5A,B), is consistent with the role of non-canonical NFĸB signaling in this model of ARVC. The gene discussed is TRAF2; the disease is Arrhythmogenic right ventricular dysplasia.