Moreover, we demonstrate that rIL-9 as such, but importantly, endogenously produced IL-9 in SF potentiates the differentiation of Th17 cells, as evidenced by (i) expression of signature transcription factor RORγt and increase in IL-17 producers in the SF of RA, (ii) blocking IL-9 present in SF of RA patients abrogates such effects in our experiments. The gene discussed is IL17A; the disease is rheumatoid arthritis.