Cystic fibrosis, the most common genetic disorder in Caucasians, is caused by autosomal recessive mutations of the cystic fibrosis transmembrane conductance regulator (CFTR), an anion channel expressed on the apical surfaces of epithelial cells in airways, pancreatic ducts and other tissues. In Europe, 1 in 2000–3000 newborns are affected by cystic fibrosis [1, 2]. CFTR mutations can be categorised into seven classes on the basis of the aberrant CFTR synthesis or function [3].
