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have demonstrated that TGF- enhances the immunosuppressive capabilities of MDSCs in non-small cell lung cancer patients by activating the mTOR/HIF-1 signaling pathway, which in turn upregulates the expression of CD39 and CD73 on MDSCs (114).We postulate that the development of small molecule inhibitors or antibodies specifically targeting HIF-1 activity, or the utilization of existing mTOR inhibitors (such as rapamycin and its derivatives), may effectively impede the activation of HIF-1 by TGF-, thereby inhibiting the recruitment and activation of MDSCs

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