The Th2 cytokines IL-4 and IL-13 were employed in various human skin models to mimic an atopic dermatitis-like Th2-driven inflammation, which results in hyperproliferation, impaired lipid composition of the cornified layer, and reduced skin protein expression; these alterations, in turn, impair keratinocyte barrier functions (25, –, 27). The gene discussed is IL13; the disease is atopic eczema.