In fact, IL-13-producing lung ILC2 were upregulated following intranasal IL-25 or IL-33 administration, or during an ovalbumin-driven model of allergic asthma [24], and adoptive transfer of wildtype, but not IL-13-deficient, ILC2 was sufficient to restore IL-25-induced AHR to otherwise resistant IL-13-deficient mice. The gene discussed is IL13; the disease is allergic asthma.