Recent advances in deciphering the complex molecular mechanisms involved in the onset and evolution of psoriasis have been translated from bench to bedside and have allowed for the development of biotherapies, i.e., monoclonal antibodies directed against some key interleukins (IL) involved in the pathogenesis of the disease: IL-12, IL-17, IL-23 and tumor necrosis factor-alpha (TNF-alpha). This evidence concerns the gene IL17A and psoriasis.