Psoriasis is an immune-mediated skin disease in which interferon (IFN)-γ, tumor necrosis factor (TNF)-α, interleukin (IL)-17, and IL-22 cytokines, released by Th1 and Th17 lymphocytes1,2, have a pathogenic action by promoting hyperproliferation, interfering with the terminal differentiation and inducing the secretion of pro-inflammation molecules by keratinocytes3,4. This evidence concerns the gene TNF and psoriasis.