In the TME, T cell proliferation is inhibited by binding with inhibitory ligands (e.g., programmed cell death ligand 1 [PD-L1] and Galectin-9] and by suppressive myeloid-derived suppressor cells, cancer-associated fibroblasts and other tumor-associated cells, which secrete factors such as VEGF and TGFβ that contribute to an abnormal TME characterized by inflammation and hypoxia (Fig. 2e) [321]. Here, VEGFA is linked to neoplasm.