Furthermore, in accordance with our hypothesis combination of CXCR4-antagonist and anti-OX40 treatment resulted in an increase in the functionality of tumor-infiltrated effector cells as determined by the numbers of total and antigen-specific granzyme B+ and IFN-gamma+ CD8+ T-cells, leading to significant delay in tumor growth and prolonged mice survival. The gene discussed is IFNG; the disease is neoplasm.