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This is challenging in the tumor microenvironment (TME), where T cells compete with tumor cells that also rely on aerobic glycolysis 6,7 , creating intense competition for glucose 4 , compounded by dysregulation of nitrogen metabolism 8,9 and reactive oxygen species (ROS)-mediated T EFF suppression 10,11

SAH levels could be decreased following Se (aqueous or SeNP) treatment, resulting in increased HMT activity, by diverting HCys into the transsulfuration pathway, as the introduction of selenite or SeNP into this pathway leads to the formation of selenoglutathione (GS-Se-SG) (Fig

Whether the use of the synthetic agonist can reverse the tumor suppression effects of the mGluR2/3 antagonist mentioned above is not well established, but it might be possible that the use of the natural ligand of mGluR2/3 and the use of the synthetic agonist can stimulate tumor cell proliferation and tumor growth in vivo