The pro-inflammatory cytokine interleukin (IL)-23 is a known key mediator of PsA pathogenesis.6, –8 IL-23 acts upon T-helper (Th) 17 cells to induce the expression of effector cytokines including IL-17, IL-21, and IL-22.9, –11 Available data indicate that IL-17 is a key factor in the development of psoriatic skin lesions,12 and IL-22, induced by IL-23 in the entheses, promotes enthesitis and pathologic bone formation.13,14 Furthermore, the production of IL-17A and tumor necrosis factor α (TNFα) within the IL-23/Th17 pathway may also lead to joint damage.14 Here, TNF is linked to enthesitis.