Genetic deletion or pharmacological inhibition of complement components such as C5 (9, 10), Factor B (8, 9) or C5aR1 (9, 12) markedly reduced the development of skin lesions (9, 18, 19) in the antibody-transfer model of EBA, which mimics the inflammatory EBA subtype. This evidence concerns the gene C5AR1 and acquired epidermolysis bullosa.