The facts that binding of PV IgGs to KCs can activate PLC, elevate DG and IP3 levels, upregulate PKC activity and increase the concentration of the intracellular free Ca2+, and that these signaling events play an important role in pemphigus pathophysiology by altering the cell-cell adhesion of KCs are well known (27, 28, 29, 30). This evidence concerns the gene TBCE and pemphigus.