Using human monocyte-derived macrophages and tumor-associated macrophages (TAMs), we show here that a combination of the inflammatory cytokines GM-CSF and IFNγ triggers glyconeogenesis from glutamine, lactic acid, and glycerol in macrophages, whereas treatment with GM-CSF or M-CSF plus IL-4 promotes glycogenesis. The gene discussed is CSF2; the disease is neoplasm.