In ABPA, consistent with allergic airway biology, persistent epithelial- and alarmin-derived signaling, together with IL-13-associated goblet cell metaplasia, MUC5AC-rich secretions, and eosinophil extracellular trap formation, likely contribute to tenacious mucus despite suppression of peripheral eosinophils [12,13]. The gene discussed is MUC5AC; the disease is allergic bronchopulmonary aspergillosis.