Probably one of the most notable examples of pharmacological rescue of misfolded membrane proteins is the case of the ΔF508 defective cystic fibrosis transmembrane conductance regulator -CFTR- for which several pharmacoperones have succeeded in restoring membrane expression and function of the mutant Cl- channel in individuals with cystic fibrosis (25, 28–33). The gene discussed is CFTR; the disease is cystic fibrosis.