However, this paradigm suffers from major limitations that include the non-response of monoclonal antibodies (mAb) against IFN-γ and CD4+ T cells in RA patients, the presence of Th17-IL-17 instead of Th1-IFN-γ positive CD4+ cells within the rheumatoid synovium, and a paradoxical IFN-γ anti-arthritis effect reported in RA-prone murine models as compared to the promotion of arthritis flares by IFN-γ in normal mice [16,17,18,19]. The gene discussed is IL17A; the disease is arthritic joint disease.