Autoantibodies directed against epitopes on the transmembrane adhesion molecules of desmosomes have been shown to be pathogenic in the intra-epithelial blistering diseases which comprise the pemphigus family [17, 18], all of which present with flaccid blisters or erosions, as a result of the loss of epidermal integrity elicited by targeting the inter-keratinocyte “glue.” The most common of these diseases, pemphigus vulgaris (PV), is primarily a disease of oral mucosal blistering and DSG3 is the principal target antigen [19]. The gene discussed is DSG3; the disease is pemphigus vulgaris.