The elevated AA/LA ratio and higher levels of the AA-derived oxylipin metabolite 15-HETE in I allele carriers support the biological plausibility of 1) the association between the presence of ≥1 I allele and increased colorectal polyp risk in untreated individuals, driven by AA-mediated pro-tumorigenic signaling by PGE2 [7], and 2) the augmented polyp prevention efficacy of EPA treatment via antagonism of enhanced FADS1-dependent AA availability in I allele carriers [11]. Here, FADS1 is linked to polyp.