In pemphigoid diseases (PDs), neutrophils are activated by IgG autoantibodies deposited at the dermal-epidermal junction. Intracellular signaling cascades induced by IgG binding to FcγRs ultimately lead to the release of effector molecules, such as proteases and ROS, resulting in skin blistering and erosions. Hence, these signaling cascades, mostly consisting of kinases, are promising therapeutic targets. B04 therefore aims to comprehensively characterize these kinase cascades and to examine the therapeutic potential of inhibitors of select kinases for PDs.