In the context of cancer, it is hypothesised that for an anti-tumour IgE to avoid triggering type I hypersensitivity, the target antigen should be found at low density, and in monomeric form, on healthy cells (and in the circulation) and/or should have only a single IgE-binding epitope, so that IgE cross-linking on the surface of effector cells or bridging with a target cell cannot be achieved [198]. The gene discussed is IGHE; the disease is neoplasm.