In the hypoxic condition, cancer cells extensively secrete VEGF-A that bind with VEGF receptor 2 (VEGFR2) and subsequently promote tumor angiogenesis through enhanced EC proliferation, increased migration via PI3K/AKT/ mammalian target of rapamycin (mTOR)/mitogen-activated protein kinases (MAPK), and increased nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) signalling pathways [181]. This evidence concerns the gene VEGFA and neoplasm.