The current paradigm of treatment for CF often entails the administration of small-molecule CFTR modulators, which include CFTR potentiators – such as ivacaftor (VX-770) – that bind to CFTR and improve its open channel probability, and correctors – such as tezacaftor (VX-661) and lumacaftor (VX-809) – that improve CFTR trafficking and localization to the apical plasma membrane. Here, CFTR is linked to cystic fibrosis.