It has been proposed that ILC2s in COPD patients may be activated by inflammatory mediators released by the pulmonary epithelium and other structural cells [52], thus resulting in the synthesis of a number of cytokines, including interleukin (IL)-4, IL-5 and IL-13, which are, in turn, known to participate in airway eosinophilia and parenchyma remodeling [53]. The gene discussed is IL4; the disease is Increased total eosinophil count.