Nonetheless, the lack of IL-4 upregulation, a classic allergic mediator, and the potentiation of a TNFα/MCP-1 axis observed with anti-tumour IgE effector functions, may point to a less dominant role for an allergic, and a more prominent IgE-driven anti-tumour mechanism normally preserved for immune defence and parasite destruction by mobilising and activating macrophages. The gene discussed is TNF; the disease is neoplasm.