The central pathophysiologic role of the IL-23/IL-17A axis in psoriasis has been confirmed by the therapeutic success with targeted monoclonal antibodies; the effect of tumor necrosis factor α (TNF) antagonists is probably exerted indirectly, since TNF is an upstream inducer of IL-23 and acts synergistically with IL-17 increasing the up-regulation of many psoriasis-related pro-inflammatory genes in keratinocytes [1]. Here, IL17A is linked to psoriasis.