Given that the restoration of either wild-type or mutant PKP2 protein was sufficient to increase desmosomal protein levels, these data highlight that loss of PKP2 protein quantity and not quality (that is, mutant form) is the driver of desmosomal disruption in PKP2 Hom neonatal cardiomyocytes and early ARVC. This evidence concerns the gene PKP2 and Arrhythmogenic right ventricular dysplasia.