PKP2 and Arrhythmogenic right ventricular dysplasia: In vivo-based AAV-PKP2 strategies were sufficient to restore PKP2 in the early stages of ARVC development in PKP2 Hom mice, which was sufficient to prevent not only the striking cardiac desmosomal dissolution but also gap junction deficits that together drive the long-term electrical (arrhythmias) and structural (cardiac pathology and biventricular dysfunction) cardiac deficits in ARVC in PKP2 Hom hearts.