Allergen-specific IgE is pathogenic in asthma, presumably by driving FcεRI-mediated degranulation and cytokine secretion, including autocrine release of IL-33 and downstream effector signalling: thus, collectively these data suggest that at least some of the in vivo protective effects of ES-62 in chronic models of asthma reflect modulation of IL-33/ST2 signalling. The gene discussed is IL1RL1; the disease is asthma.