Although several mouse models have been used for the study of IBD and CAC, the majority of these models rely either on genetic alteration of colorectal cancer pathways (e. g., Wnt–β-catenin or IL-6-STAT3 pathways), modulation of factors involved in the mucosal immune response (e. g., IL-2 or IL-10 deletion), or treatment with carcinogens, particularly AOM. This evidence concerns the gene STAT3 and inflammatory bowel disease.