In mice, cigarette smoke exposure leads to an increase in all ILC subpopulations in bronchoalveolar lavage fluid, particularly IFN γ+ and IL-17+ ILC.IL-17 is considered a key driver of neutrophil inflammation in COPD (133), inducing neutrophil maturation and recruitment, and through the release of its proteolytic enzymes (elastase, histone G, and protease-3), facilitating Sputum IL-17 is higher in COPD patients than in non-smoking controls, and bronchial biopsies from COPD patients also show increased expression of IL-17, IL-22 and IL-23. The gene discussed is CCL27; the disease is chronic obstructive pulmonary disease.