Preoperative administration of the antiinflammatory NSAID ketorolac and the SPM called resolvin increases disease-free survival rates and prevents metastasis in mouse tumor models. Ketorolac inhibits the COX-1 pathway and formation of platelet aggregation by blocking TXA₂ production. COX-2/PGE₂ activity is required when ketorolac is administered preoperatively. Ketorolac also increases the production of an SPM called lipoxin A (LXA₄) that plays a role in the antitumor function of ketorolac. Resolvins are produced from omega-3 fatty acid metabolism; however, in this study, resolvins were exogenously administered at the preoperative stage and increased cancer-free survival in mouse models. Preoperative ketorolac administration increased CD4⁺ and CD8⁺ T cells and immunological memory, decreased Foxp3⁺ regulatory T cells, and exhausted T cells in the spleen. These immunological changes mediate the antitumor action of this inhibitor. PGs, prostaglandin E2, D2 and F2 alpha; PGI₂, prostacyclins; LOX, lipoxygenase; EPA, eicosapentaenoic acid; DHA, docosahexaenoic acid.