Upon receiving dominant proangiogenic stimuli from malignant cells or the tumor microenvironment through several effectors, such as vascular endothelial growth factors (VEGFs), platelet-derived growth factor (PDGF), placenta-derived growth factor (PlGF), hypoxia-inducible factor-1 (HIF-1α), angiopoietin-2, transforming growth factor β (TGF-β), or interleukin-8, ECs from preexisting vessels become activated. Here, VEGFA is linked to neoplasm.