On one hand, it has been postulated that a mechanism for the presence of anti-DSG2-abs in ARVC is the exposition of DSG2 cryptic epitopes [26] after desmosome disruption; on the other hand, in ARVC, several mutations in different desmosomal proteins can be found, and in most cases the disease remains genetically elusive, i.e., without the possibility to identify a pathogenic mutation at genetic screening. This evidence concerns the gene DSG2 and arrhythmogenic right ventricular cardiomyopathy.