Based on the current mechanistic understanding that the n–3 HUFA EPA competes with its n–6 HUFA counterpart AA and inhibits protumorigenic signaling by downstream lipid mediators such as PGE2, we performed a secondary analysis of the seAFOod trial to test the hypothesis that the FADS Indel I allele, which drives FADS1-dependent AA synthesis and bioavailability, predicts colorectal polyp prevention efficacy of EPA. Here, FADS1 is linked to polyp of large intestine.