Recently, sequencing of the exons and flanking introns of the genes encoding the α, β, and γ subunits of ENaC in twenty non-classic CF patients, that is patients with bronchiectasis and elevated sweat chloride concentrations but without two CFTR mutations, identified in four patients five missense mutations (one in ENaCα and four in ENaCβ) and one splicing mutation in the 3' splice site of ENaCβ intron 12 [13]. Here, CFTR is linked to cystic fibrosis.