To explore further whether IL-23 might be linked to GM-CSF, TNF, and/or CCL17 in the control of arthritic pain and disease, we again utilized arthritis models which are driven by each of these cytokines individually in a lymphocyte-independent manner [5, 8, 9]—these other monoarticular arthritis models all involve systemic administration of a cytokine into a mouse with a methylated BSA (mBSA) “primed” joint and are a convenient approach to explore potential pathways downstream of a particular cytokine [8, 9]. The gene discussed is TNF; the disease is Arthritis.