Stat3 signaling also plays critical roles in a mouse model of IBD, i.e., genetic ablation of Stat3 in CD4+ T cells contributed to the defect of Th17 cell differentiation and then were unable to induce intestinal inflammation during the development of T cell-mediated colitis, suggesting a critical role for T cell-intrinsic Stat3 in the progression of colitis. This evidence concerns the gene STAT3 and colitis.