IFN-γ directly targets and inhibits signal transducer and activator of transcription 3 (STAT3) by upregulating the expression of miR-125a and miR-125b, thereby inhibiting T helper 17 (Th17) differentiation and enhancing the ability of BMMSCs-Exo to improve the colitis phenotype in mice (193). This evidence concerns the gene STAT3 and colitis.