Individuals who have inherited two mutated copies of the CFTR gene produce an altered CFTR protein (with decreased or absent CFTR chloride channel activity) that inhibits the flow of water and chloride ions across the cellular membranes and triggers the onset of clinical phenotypes characterized by an altered sweat test, pancreatic insufficiency, and pulmonary infections that gradually lead to respiratory insufficiency [1,2]. This evidence concerns the gene CFTR and exocrine pancreatic insufficiency.