We suggest that inhibiting TGFB2 production and release from immunosuppression in pbDMG tumors with the concurrent activation of M0-derived anti-tumor CD86-expressing M1 macrophages via interferon-gamma (IFN-γ) may promote proinflammatory cytokine synthesis, enhanced phagocytosis, and increased tumor antigen-presenting capacity to improve the anti-tumor response [35]. This evidence concerns the gene CD86 and neoplasm.