2015), in which CS caused a transient disruption in the airway epithelial barrier integrity, accompanied by minor cytotoxic effects measured at the apical surface. Both sIL6R and AREG were barely detectible in the apical washes collected from ALI‐PBEC of 17 COPD donors at different stages of disease, following exposure to either CS or air (Fig. 1A and B). This evidence concerns the gene IL6R and chronic obstructive pulmonary disease.