The pathogenesis of EB includes infiltration of inflammatory cells such as eosinophils, Th2/Th17/Treg and mast cells, and the high expression of inflammatory cytokines and mediators, including interleukin (IL)-4, eotaxin, IL-5, IL-13, IL-17A, IFN-γ, IL-1β, IL-6, TNF-α, histamine, leukotrienes, prostaglandin E2 (PGE2), PGD2 and oxidative stress2,5–17. This evidence concerns the gene IL4 and epidermolysis bullosa.