data from bronchial brush samples implicated that the lung pathology in CF is predominated by Th17 and Th1 gene signatures (43), the increased pulmonary presence of the ILC2-activating cytokine IL-33 and augmented levels of the type-2 effector cytokines IL-5, IL-9, and IL-13 in CF BAL and sputum samples as well as the upregulation of local Th2 responses upon chronic infections with Pseudomonas aeruginosa in CF patients strongly argued for a potential, albeit less elucidated, involvement of ILC2s in CF pathogenesis (13, 14, 42, 44–46). This evidence concerns the gene SGCG and cystic fibrosis.