Adult MUC5B-deficient mice displayed bronchial hyperplasia and metaplasia, interstitial thickening, alveolar collapse, immune cell infiltrates, fragmented and disorganized elastin fibers, and collagen deposits that were, for approximately one-fifth of the mice, associated with altered pulmonary function leading to respiratory failure demonstrating that the mouse MUC5B is essential for maintaining normal lung function (Valque et al., 2019). This evidence concerns the gene MUC5B and respiratory failure.