VEGF can bind to receptors VEGFR-1 and VEGFR-2 on the surface of vascular endothelial cells, induce receptor dimerization, and phosphorylate the receptors’ intracellular tyrosine kinase structure domain activation, activate PLC-γ/PKC, RAS/MAPK and PI3K/AKT signaling pathways, induce endothelial cell proliferation, migration and cell survival (48–51), and ultimately lead to tumor angiogenesis (52). Here, AKT1 is linked to neoplasm.