A large body of literature, in both animal models of experimental arthritis and human disease, demonstrates the critical contribution of pro-inflammatory CD4+ T helper cell subsets to pathogenesis, with particular roles for their signature cytokines IFNγ (produced by Th1 cells), IL-17A (produced by Th17 cells) and TNFα (produced by both Th1 and Th17 cells, as well as monocytes/macrophages) (reviewed in [2]). This evidence concerns the gene IFNG and arthritic joint disease.