The pathological role of IL-33 is most firmly established in the case of asthma, supported by a large body of experimental data ranging from transgenic overexpression or local intra-tracheal administration of recombinant IL-33, IL-33 or ST2 gene ablations, and pharmacological inhibition of the IL-33 signaling pathway in mice (11, 12). The gene discussed is IL33; the disease is asthma.