The colitogenic potential of IFN-γ-producing Th17 was verified by a study focusing on IFN-γ-deficient Th17 cells, which retained an IL-17A+ phenotype and were unable to induce colitis in a Th17-transfer colitis model, while development of disease required the transition of Th17 precursors to Th1-like cells depending on the expression of both STAT4 and T-bet [158]. This evidence concerns the gene STAT4 and colitis.