However, our blocking of TGF-β1 signalling apparently did not sufficiently suppress the formation or activity of Th17 cells, as arthritis pathology was not affected by local SB-505124 treatment, showing that our strategy to target the Th17 pathway upstream is not as effective as blocking the main effector cytokine IL-17 itself. Here, TGFB1 is linked to arthritic joint disease.