Activation of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice.