We observed that macrophages tend to localize at the periphery of the MTS; MTS treatment with a combined CSF1R kinase inhibitor and an activating anti-CD40 mAb increased M2 over M1 pro-tumoral phenotype (CD163/CD86 and CD206/CD86 marker ratios), abrogated G2/M phase transition of cancer cells, promoted the production of TNF-α and reduced cancer cell viability. The gene discussed is CD86; the disease is cancer.