It has been commonly accepted that classically activated M1 macrophages suppress tumor growth and progression by production of reactive oxygen species (e.g., nitric oxide), whereas alternatively activated M2 macrophages promote tumor growth and progression by releasing growth factors (e.g., epidermal growth factor, fibroblast growth factor 1, vascular endothelial growth factor A) [9, 13–16]. This evidence concerns the gene EGF and neoplasm.