In mice, it has been recently demonstrated that MUC5B overexpression in bronchoalveolar epithelia is related to impaired mucociliary clearance (MCC), indicating excessive retention of inhaled substances (air pollutants, particles and chemicals from cigarette smoke, microorganisms, etc.)or endogenous inflammatory debris, which causes a reactive or regenerative fibrotic response localized to the bronchoalveolar region and promotes lung fibrosis development [84,85]. This evidence concerns the gene MUC5B and pulmonary fibrosis.