The pathogenesis of AD is known as the abnormal activation of T helper 2 (Th2) lymphocyte, which can subsequently secrete a series of pro-inflammatory cytokines including immunoglobulin E (IgE), interleukin-4 (IL-4), IL-5, IL-13, IL-17, IL-22, IL-31, and thymic stromal lymphopoietin (TSLP), leading to epidermal barrier defect and increased skin inflammation (7–9), whereas psoriasis is mainly considered the abnormal activation of Th1 and Th17 lymphocytes which secrete pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interferon-γ (IFN-γ), IL-17, and IL-23 (10). This evidence concerns the gene IL17A and psoriasis.