To determine the role underlying the increased survival after radiation treatment in mice implanted with CXCR4 knockdown GL26-Cit-Sh2CXCR4 cells, we analyzed tumor sections from non-irradiated vs irradiated groups of mice for cleaved caspase-3, a major downstream effector mechanism for caspase-mediated apoptotic cell death. The gene discussed is CXCR4; the disease is neoplasm.