We believe that the minimal variance from normal controls and pemphigus patients in the levels of non-DSG autoAbs, coupled with the lack of variation with treatment and the lack of correlation with IgG anti- DSG1 and -DSG3 autoAb levels and clinical improvement suggests that these Abs may not play a direct role in the pathogenesis of the disease in our patient population. The gene discussed is DSG3; the disease is pemphigus.