CRC-like ontogenesis in db/db mice, and the expression of β-catenin and HNF-4α-responsive genes, reverted all to the wild-type phenotype, by crossing the db/db mice with the fat-1 transgene that encodes an (n-6) to (n-3) PUFA desaturase [14], resulting in colonic (n-3) PUFA enrichment. This evidence concerns the gene FAT1 and colorectal carcinoma.