High risk of CRC promotion by diabetes has indeed been indicated by our previous study whereby colonic ontogenesis in db/db mice displayed CRC-like features with increase in proliferation and de-differentiation of epithelial colonocytes and goblet cells, being driven by increase in the expression and transcriptional activities of colonic HNF-4α and β-catenin/Tcf [13]. This evidence concerns the gene HNF4A and diabetes mellitus.