Previous chemoprevention studies in the field have focused on non-steroidal anti-inflammatory drugs (NSAIDs), which are associated with reduced EAC incidence in BE patients.[8–10] NSAIDs inhibit prostaglandins through suppression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2),[11] the latter of which is overexpressed in BE and EAC.[12] Prostaglandin E2 (PGE2), a pro-inflammatory prostaglandin regulated by the COX-2 pathway, has been associated with proliferation[13] and cellular migration[14] in BE and EAC. The gene discussed is PTGS2; the disease is Barrett esophagus.