To realize these aims, we assessed the impact of the drug on: (i) the extent of COX-1 acetylation at Serine529 (primary endpoint) and COX-2 acetylation at Serine516 in colorectal adenomas, normal mucosa, and platelets; (ii) the systemic biosynthesis of prostanoids; (iii) the expression of enzymes and receptors of prostanoid pathways in platelets and intestinal tissue; and (iv) proteomics of FAP patients’ adenomas. This evidence concerns the gene PTGS1 and Familial adenomatous polyposis.