Furthermore, T2 cytokine-induced CCL26 secretion was significantly higher in BECs from asthma patients as compared with cells from healthy donors, and since CCL26 is a chemokine critically involved in recruiting eosinophils to the airways, a key feature of airway inflammation in T2-high asthma (24), it emerges as another crucial driver of airway inflammation and hyperresponsiveness targeted by anti-IL-4Rα therapy. The gene discussed is IL4R; the disease is asthma.