Asthma is an allergic inflammatory disease driven by type 2 (T2) and non-T2 immune pathways, resulting in diverse phenotypes and varying levels of severity.1, 2, 3 IL-33, thymic stromal lymphopoietin, and IL-25, primarily derived from bronchial epithelial cells, regulate IL-4, IL-5, and IL-13, contributing to the development of treatment-resistant T2 inflammatory asthma.4 The gene discussed is IL5; the disease is asthma.