Secreted gel-forming mucins (1) are key components of mucociliary transport, a vital airway innate defense mechanism (2). Mucin and mucus alterations are present in asthma (3), cystic fibrosis (4), and chronic bronchitis (5), and mucin gene polymorphisms are also implicated in the pathogenesis of idiopathic pulmonary fibrosis (6). Increased numbers of mucin-producing goblet cells at locations where they are normally present (hyperplasia) or absent (metaplasia) are pathognomonic responses of the airways to diverse environmental stimuli. Although they are clearly important and protective at homeostatic levels, mucin and mucus are likely harmful when produced in excess, as most vividly and tragically illustrated in fatal asthma (Figure 1). Importantly, specific therapies targeting mucin hypersecretion in asthma and other lung pathologies are not currently available
