Upon exposure to intracellular GSH and H2O2, the K1 prodrug was activated inside the tumor cells to release SN‐38 and indomethacin.[165] SN38 suppressed tumor growth by inducing apoptosis of the tumor cells, while indomethacin relieving the immunosuppressive tumor microenvironment by suppressing intratumoral secretion of proinflammatory cytokines TNF‐α and IL‐6, and enhancing the production of IL‐10 (anti‐inflammatory cytokine).[165]. This evidence concerns the gene TNF and neoplasm.