Autoimmune bullous diseases (AIBDs) exhibit an immunoglobulin (Ig) G and/or IgA antibody response to various cutaneous autoantigens.1 Immunoglobulin G antibasement membrane zone autoantibodies in bullous pemphigoid (BP) sera react with BP180 and BP230.1-4 While the pathogenic role of BP180 was confirmed by various disease models,5,6 production of autoantibodies to BP230 was considered an epiphenomenon. The commercial availability of IgG enzyme-linked immunosorbent assays (ELISAs) for both BP180 and BP230 makes it possible to more closely examine this premise.3,4