Though the pathophysiology of psoriasis/PsA is complex and remains incompletely understood (5), the role of effector CD4+ T-cells has been established (6), and pathological activation of the Tumor Necrosis Factor (TNF)/Interleukin (IL-)23/IL-17 cytokine axis contributes to the differentiation and activation of effector T-cells and their accumulation in affected tissues (7–9). This evidence concerns the gene TNF and psoriasis.