One explanation is that immune cells initially recognize dysplastic tissue and mount an inflammatory response at the premalignant stage, but factors released from the developing lesion, including G-CSF and PGE2, simultaneously recruit a population of immunosuppressive cells, which secrete factors such as IL-10 and TGF-β to dampen an effective Th1-mediated response as the tumor is established. The gene discussed is CSF3; the disease is neoplasm.