Of note, profiles of cell proliferation, differentiation and the expression and activity of HNF-4α and β-catenin reported here for carcinogen-induced CRC in db/db, fat-1 and fXB mice are similar to those previously reported for colonic ontogenesis of respective mice [13], implying that HNF-4α and β-catenin may act as colonic ontogenic and oncogenic drivers in the diabetes context. This evidence concerns the gene HNF4A and colorectal carcinoma.