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As a consequence of tumor metabolism, additional effects arise from the mechanisms involved in HIF-1α expression, including the inhibition of CD8⁺ T cells—mediated by mTOR-driven accelerated glycolysis—and the recruitment of Tregs through the chemokine (C-C motif) ligand 20 (CCL20)/C-C chemokine receptor type 6 (CCR6) axis [14, 43]