Previous studies reported that the modification of O-GlcNAcylation of Stat3 at the Thr717 residue suppresses its phosphorylation and the expression of the downstream anti-inflammatory cytokine IL-10 and contributes to the augmented disease severity in azoxymethane (AOM)-induced colitis and colitis-associated cancer, whereas myeloid-derived cullin 3 promotes Stat3 phosphorylation by inhibiting OGT expression and protects against intestinal inflammation [66]. Here, STAT3 is linked to inflammation.