Epidermolysis bullosa acquisita (EBA) is an autoimmune blistering disease characterized by spontaneous or trauma-induced blisters that heal with scarring. Immunologically, EBA is characterized by the deposition of IgG directed against anchoring fibrils in the sublamina densa of the basement membrane zone. On indirect immunofluorescence, IgG EBA antibodies bind the base of salt-split skin, differentiating EBA from bullous pemphigoid.1 IgM, IgA, complement, and properdin may also sometimes be found at the basement membrane zone, but only in modest amounts.