The findings that increased release of IL‐18 by airway macrophages is associated with both the acute and chronic forms of hypersensitivity pneumonitis 13, that IL‐18 is located in neutrophils 14 and facilitates neutrophil transmigration 15, that IL‐18 down‐regulates B‐cell migration 16, and that virus antigen EBNA2 induces expression of IL‐18R in B cells 17 implicate that macrophage, neutrophils and B cells may participate in the development of airway inflammatory disorders including asthma via a IL‐18‐related mechanism. The gene discussed is IL18R1; the disease is asthma.