It is possible that GAMs may be in a state of being alternatively activated upon recruitment by tumor cells (e.g., TGF-β) that aid tumor growth at the leading edge, but are subsequently metabolically switched to an inflammatory state in the hypoxic necrotic center via HIF-1α signaling and become part of the necrotic mass [20,24]. The gene discussed is TGFB1; the disease is neoplasm.