In this line of thoughts, the direct inhibition of Dsg3 binding together with the signaling of p38MAPK, Src, EGFR, and caspase-3 would be sufficient to cause mucosal erosions (Figure 1), whereas additional mechanisms such as Ca2+, which has been shown to be associated with PKC activation in keratinocytes treated with pemphigus antibodies (68, 69), as well as Erk would be required for epidermal blistering. The gene discussed is DSG3; the disease is pemphigus.