Furthermore, the hypoxic tumor environment upregulates the expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1 alpha (HIF1α) in glioma cells, which then induces ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2) and aids in the accumulation of MDSCs by converting extracellular ATP to 5′-AMP [42]. Here, HIF1A is linked to neoplasm.