HIF1A and neoplasm: Simultaneously, hypoxia microenvironment increases the demand for tumor angiogenesis through hypoxia-inducible factor-1α (HIF-1α)-mediated up-regulation of various growth factors (represented by VEGF) [166], which in turn activates the FasL on tumor endothelial cells, thus triggering apoptosis in T cells upon binding to Fas expressed on T cells and reducing T cell infiltration [167].