The importance of an impaired epidermal differentiation process and skin barrier dysfunction in the pathogenesis of AE has recently been emphasized when a set of so-called “epidermal differentiation genes”, including S100A7, S100A8, loricrin and filaggrin (FLG), was found to be differentially expressed in AE patients compared to healthy control individuals [14]. The gene discussed is FLG; the disease is acrodermatitis enteropathica.