In p50 deficient mice or with restricted deficiency in bone marrow cell, it retards the growth of melanoma (B16) and fibrosarcoma (MN/MCA1) tumors.168 The evidence suggests that there is an immune-suppressor switch that promotes the change of populations of anti-tumor immune cells, such as M1, to populations of immunosuppressive cells such as M2 macrophages.167 The polarization of macrophages could be a therapeutic target, establishing immunotherapies for the accumulation of M1 macrophages with tumoricidal functions by recruiting and preventing their desensitization and switching to M2. The gene discussed is NFKB1; the disease is neoplasm.