Several studies have shown that small organic compounds which stabilize PM protein [98] can rescue protein folding defects by increasing traffic and function at the PM for selective mutants on the cystic fibrosis-related CFTR chloride channel [98,271], aquaporin-2 water channel (AQP2), and V2R associated with nephrogenic diabetes insipidus (NDI) [272,273]. This evidence concerns the gene AQP2 and cystic fibrosis.