Significantly fewer IL-17–producing cells were generated from SKG Ptpn22−/− CD4 T cells than from SKG mice (Fig. 7D, 7E), suggesting that loss of PTPN22 produces an inherent bias against polarization to the IL-17 lineage that may contribute to the reduction in susceptibility to arthritis observed in this strain of mice. The gene discussed is IL17A; the disease is arthritic joint disease.