Early ILC2 studies using mouse models of asthma with protease-derived allergens demonstrated that damaged airway epithelial cells release cytokines that include IL-25, IL-33, and thymic stromal lymphopoietin (TSLP), which directly and potently activate ILC2s, leading to production of IL-4, IL-5, IL-9, and IL-13 [1,2]. The gene discussed is IL4; the disease is asthma.