The development of keratinocyte dissociation pemphigus models allowed for the identification of several signaling pathways (e.g., p38 mitogen-activated protein kinase (MAPK), phospholipase C (PLC)/protein kinase C (PKC) activation), with different steps of desmosome turnover after pemphigus autoantibodies engage desmosomal targets [5,6]. This evidence concerns the gene HSPG2 and pemphigus.