In consistent with the changes of Pou2f3 in the IBD animal model, the expansion of Dclk-1+tuft cells in crypt were significantly inhibited after DSS induction, while TSG-6 treatment notably enhanced Dclk-1+tuft cells proliferation, which coincided with improvement of intestinal barrier function and reduction of proinflammatory mediators. Here, DCLK1 is linked to inflammatory bowel disease.