However, this did not result in suppression of arthritis, suggesting that (1) the Th17 pathway is not that important in this model, (2) TGF-βRI is redundant and TGF-βRII/III and Smad-independent signaling continues, (3) the remaining (Th17) cells are highly active due to loss of TGF-β1-mediated dampening, or (4) that the treatment with SB-505124 had a too limited duration in time on TGF-β1 signaling to suppress the arthritis measured at end stage of our in vivo experiment. The gene discussed is TGFB1; the disease is Arthritis.