Pemphigus vulgaris (PV) is a severe autoimmune skin blistering disease in which autoantibodies against desmoglein 3, among others, lead to its internalization and the apoptolysis of keratinocytes. Since the underlying signaling events are not yet completely understood, the aim of this project is to validate signal inhibitors used in previous projects and prove their influence on the internalization of desmoglein 3 after incubation with PV autoantibodies.