This third line of evidence that the relative contribution of various signalling pathways for skin blistering in pemphigus is different comes from studies in human skin ex vivo where inhibition of p38MAPK, ERK, and PLC activity as well as of Ca2+ influx were sufficient to abrogate skin blistering whereas inhibition of Src and PKC was not (182, 191, 215, 220, 229). The gene discussed is PRRT2; the disease is pemphigus.