Protein-array profiling indicated that CXCL12 silencing broadly reduced pro-tumor mediators in CAF-conditioned medium (e.g., IL-6, TGF-β1, VEGF, FGF, EGF, and MCP-1) while increasing anti-angiogenic factors such as serpin B5 and thrombospondin-2. The gene discussed is CCL2; the disease is neoplasm.