Although the mechanisms remain to be investigated in detail, one possible mechanism could relate to its interactions with the desmosomal resident protein CSN6, which is thought to interact with PKP2 and DSP and restrict desmosomal protein degradation, as well as circumvent ARVC and premature death in mice28, and thus improve desmosomal protein half-life over time. The gene discussed is COPS6; the disease is Arrhythmogenic right ventricular dysplasia.