Tumor-derived TGF-β stimulates CD39 and CD73 expression, thereby inhibiting NK cell and T cell functions and protecting tumor cells from the cytotoxic effect of chemotherapy via ectonucleotidase activity, where TGF-β triggers the phosphorylation of mTOR and the subsequent activation of HIF-1α to facilitate the expression of CD39/CD73 on MDSCs. This evidence concerns the gene HIF1A and neoplasm.