A large body of experimental evidence supports that hypoxia-mediated or -independent increases of HIF-1α plays critical roles in tumorigenesis and progression of many cancers via HIF-1α-dependent activation of genes that promote cancer cell survival or proliferation (such as BCL-xL), spread (e.g., CXCR4), and angiogenesis (e.g., VEGF) [26–29]. This evidence concerns the gene VEGFA and cancer.