A major unresolved question is whether the loss of cell-cell adhesion triggered by pemphigus IgG is caused by direct inhibition of desmoglein cis or trans interactions (steric hindrance), by endocytosis of cell surface Dsg3, by the activation of cellular signaling pathways, or by some combination of these events [11]–[13]. This evidence concerns the gene DSG3 and pemphigus.