We and other investigators demonstrated that IL-25, IL-33 and TSLP are crucial for development of OVA-induced “acute” airway inflammation and/or hypersensitivity—which are widely considered to be models for asthma—using mice deficient in those cytokines or mice treated with neutralizing antibodies/reagents for them [10], [20], [23]-[26]. The gene discussed is TSLP; the disease is asthma.