Depending on the stimulus and the microenvironment, TAMs can phenotypically differentiate into either “alternatively activated” M2-macrophages with pro-tumorigenic properties driven by tumor derived environmental factors such as IL-10 and IL-4 or “classically activated” M1-macrophages, which are characterized by a pro-inflammatory phenotype, showing increased expression of HLA-DR and enhanced production of IL-12 and IL-6 [5, 6]. The gene discussed is IL10; the disease is neoplasm.