Cystic fibrosis (CF), an autosomal recessive progressive condition triggered by a mutation in the gene encoding the CF transmembrane (CFTR), is characterized as chronic obstructive pulmonary disease, exocrine pancreatic insufficiency, and elevated sodium and chloride concentrations in sweat.1 Electrolyte imbalance on both sides of the membrane decreases the volume of water in the secretions of the apocrine glands, which are very viscous and result in the narrowing of the duct, blockage, and subsequent dissolution of these glands. This evidence concerns the gene CFTR and chronic obstructive pulmonary disease.