The high concentration of these mediators, notably arachidonic acid (AA), upregulates the cyclooxygenase 2 (COX-2) pathway and its terminal product prostaglandin E2 (PGE2) (5, 6), promoting chronic inflammation, and stimulating the growth of surviving tumor cells, epithelial-mesenchymal transition (EMT), and the activity of immunosuppressive cells, as well as inhibiting antitumor response (4–6). The gene discussed is PTGS2; the disease is neoplasm.