Furthermore, the group of Saffitz showed the implication of IL-17 in disruption of desmosomal proteins, i.e., translocation of plakoglobin from cell-cell junction resulting in granulomatous myocarditis as potential pathogenic links to arrhythmogenic right ventricular cardiomyopathy (ARVC) (14). This evidence concerns the gene IL17A and Arrhythmogenic right ventricular dysplasia.