The authors of the phase I/II clinical trial postulated the hypothesis that hypoxia-induced SDF-1α secretion after radiotherapy causes infiltration of bone marrow-derived macrophages/monocytes into the glioblastoma tumor via interactions between SDF-1α and CXCR4 and/or CXCR7 receptors that are expressed on the macrophages/monocytes, resulting in vasculogenesis and tumor recurrence [42,43,44]. The gene discussed is CXCL12; the disease is neoplasm.