Background: Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohns disease (CD), are associated with chronic relapsing inflammation of the intestinal tract of unknown etiology.As one of pro-inflammatory cytokines, Interleukin-17(IL-17) signaling activates the MAPK and the NF-κB pathways via IL-17RA, increases the expression of inflammatory cytokines and inhibits the function of Thl cell in IBD[1].Actl, the direct adapter protein of IL-17RA, is involved in the activation of NF-κB and PI3K pathways in an independent but indispensable manner[2].However, via which molecules and by which mechanisms Actl functions in the IL-17-mediated activation of colonic epithelial cells in the progression of IBD remain far more than clear.