T2-high asthma is mediated either by the adaptive immune response to allergens—resulting in interleukin (IL)-4, IL-5, and IL-13 production—or by innate immune activation through stimuli such as viruses, bacteria, or irritants, which trigger the release of IL-33, IL-25, and thymic stromal lymphopoietin (TSLP) from airway epithelial cells [1]. The gene discussed is IL5; the disease is asthma.