Moreover, DSS-treated Golm1−/− mice showed elevated p65 and STAT3 phosphorylation (Fig. 2j), which are indicative of robust activation of the NF-κB and IL-6/STAT3 signaling pathways, respectively.24 Taken together, the enhanced inflammatory responses in Golm1−/− mice with DSS-induced colonic epithelial damage may contribute to colitis and its progression to CAC. This evidence concerns the gene GOLM1 and colitis.