MEDICA analogs have previously been reported to ameliorate T2D in animal models [16-19], and to mimic (n-3) PUFA activity in suppressing HNF-4α transcriptional activity [15, 20], prompting our interest in probing their efficacy in preventing the development of diabetes-promoted CRC, as compared with fat-1. Here, HNF4A is linked to type 2 diabetes mellitus.