The pathogenesis of dermatitis involves epidermal barriers abnormalities, leading to heterogeneous immunological dysregulations predominantly in type 2 immunity (Th2, IL-4, IL-13, IL-31), but also including varying degrees of upregulation of the Th1 (IFN-γ), Th17 (IL-17), and Th22 axes (IL-22) (100). This evidence concerns the gene IL31 and skin disorder.