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]. The gene discussed is CXCR4; the disease is cancer.