PKP2 and Arrhythmogenic right ventricular dysplasia: Tissue collection at the end of the study and weekly monitoring showed disruption of desmosomes and GJs (Fig. 3a and Supplementary Fig. 3), high burden of spontaneous premature ventricular contractions (PVCs) (Fig. 3b) and occurrences of non-sustained ventricular tachycardia (NSVT) (Supplementary Fig. 4), biventricular dilatation (Fig. 3d), and a sharp decline in cardiac function (Fig. 3c) and survival (Fig. 3e) after 3–4 weeks of induced cardiac knock-out of Pkp2. These phenotypes recapitulated human ARVC clinical manifestations.