Current knowledge suggests that robust activation of the T-helper (Th)-2 [interleukin (IL)-4, IL-5, IL-13, IL-31] and Th22 (IL-22) immune responses in both skin and serum play a pivotal role in the immunopathogenesis of AD especially at the acute stage, followed by a variable degree of Th1[interferon-γ (IFN-γ), tumor necrosis factor alpha (TNF-a)] and Th17 (IL-17) activation in chronic disease [1,2]. The gene discussed is IL31; the disease is Alzheimer disease.