Indeed, CFTRpotentiators improve channel opening and ion transit, while correctorsenhance CFTR folding and functional insertion into the cell membrane.Thereby, patient therapy depends on CFTR-specific mutation, thus makingCF a pathology suitable for personalized medicine.6 Animal models fail in reproducing important phenotypicmanifestations of human CF disease, imposing limitations on translationalresearch. The gene discussed is CFTR; the disease is cystic fibrosis.