AKT1 and neoplasm: On one hand, apatinib selectively competes for the ATP-binding site of VEGFR-2, blocks VEGFR-2 phosphorylation, and inhibits tumor neovascularization by suppressing downstream signaling pathways, including RAF/MEK/ERK pathway, p38-mitogen-activated protein kinase (MAPK) pathway, and phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway (24, 25).