Mutations in CF can be divided into six different classes: (i) defective synthesis of full-length protein, (ii) defective protein processing and trafficking, leading to retention in the ER and degradation, (iii) defective channel opening (gating), (iv) reduced chloride permeability, (v) reduced synthesis of CFTR protein, or (vi) reduced cell-surface stability (Welsh & Smith, 1993; Castellani et al, 2008). Here, CFTR is linked to cystic fibrosis.