In two independent murine models of ARVC, systemic delivery of PKP2 via viral vectors restored plakophilin-2 expression, resulting in significant improvements in left ventricular ejection fraction, attenuation of fibrotic remodeling, suppression of arrhythmic burden, and enhanced overall survival—even when therapy was initiated after the onset of overt disease phenotypes [117]. This evidence concerns the gene PKP2 and Arrhythmogenic right ventricular dysplasia.