In line with that, CRC-like colonic ontogenesis in obese diabetic db/db mice, driven by increase in the transcriptional activity of colonic HNF-4α, was accompanied by robust increase in HNF-4α-bound (n-6) PUFA at the expense of decrease in HNF-4α-bound (n-3) PUFA [13]. The gene discussed is HNF4A; the disease is colorectal carcinoma.