Even though TNF and GM-CSF are not required in this model [9], interestingly, arthritic pain was again not seen in Il23p19−/− mice (Fig. 4); as measured histologically, Il23p19−/− mice were also protected from CCL17-driven arthritis development (P = 0.0002, 95% CI 1.501, 5.332). This evidence concerns the gene CCL17 and arthritic joint disease.