These aspects are peculiar of the DSC3/DSG3 model, given that no significant infiltration of inflammatory cells was observed in the early stages of developing blisters in the DSG3 active pemphigus mouse model (14), indicating the uniqueness of our model and a cooperation of the different auto-Abs in the induction of the pemphigus phenotype (5, 6). The gene discussed is DSC3; the disease is pemphigus.