In an orthotopic glioblastoma mouse model, hypoxia induces upregulation of CXCL12 leading to the recruitment of CXCR4-positive bone marrow derived monocytes that stimulate the formation of new tumor blood vessels—vasculogenesis (15–17), and hypoxia is a well-known inducer of VEGF expression, leading to the induction of angiogenesis and tumor progression (18). Here, CXCR4 is linked to neoplasm.