Our data indicated that the anticancer effect of rSmeg-hMIF-hIL-7 in tumor-bearing mice could be mediated mainly by two major mechanisms: attenuation of MIF signaling by interaction with CD74, perhaps via anti-MIF antibody-mediated reduction of MIF levels or neutralization of MIF activity, and attenuation of the CD4+ or CD8+ T cell mediated immune response against MIF, particularly the CD8+ T cell mediated CTL response in tumor microenvironments. The gene discussed is CD8A; the disease is neoplasm.