We have reported previously, using Il23p19−/− mice, that IL-23 is required for TNF-, GM-CSF- and CCL17-driven arthritic pain and disease development [3], indicating possible links between IL-23 and these cytokine mediators, which in turn have themselves been linked in the mBSA/cytokine arthritis models [3, 14, 15] and elsewhere in other models [14]. This evidence concerns the gene IL23A and arthritic joint disease.