In this work, we focused on increasing the M1-to-M2 macrophage and the Th1-to-Th2 helper cell ratios by injecting anti-tumor polarized cells (M1 macrophages and Th1 helper cells) and by disrupting pro-tumor positive feedback loops driven by TGF-β, IL-4 and IL-10. The gene discussed is IL4; the disease is neoplasm.