To develop potential therapeutic modalities to inhibit MCP-1 production in tumor microenvironments (TMEs), we previously analyzed the crosstalk between 4T1 breast cancer cells and macrophages and identified cancer cell-derived granulocyte-macrophage colony-stimulating factor (GM-CSF/CSF2) as a potential key molecule that regulates high-level MCP-1 production in breast cancer TMEs. The gene discussed is CCL2; the disease is neoplasm.