have demonstrated that TGF-β 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-1α activity, or the utilization of existing mTOR inhibitors (such as rapamycin and its derivatives), may effectively impede the activation of HIF-1α by TGF-β, thereby inhibiting the recruitment and activation of MDSCs. This evidence concerns the gene TGFB1 and non-small cell lung carcinoma.