The hypoxic tumor environment induces overexpression of hypoxia-inducible factor-1 (HIF-1), which subsequently promotes the upregulation of immunosuppressors such as vascular endothelial growth factor (VEGF), IL-10, transforming growth factor beta (TGF-β), galectin-1, COX-2, and programmed death ligand 1 (PD-L1), thereby contributing to tumor progression and metastasis [48,49]. Here, VEGFA is linked to neoplasm.