27, 110) since these drugs can correct the basic defects of the mutant CFTR protein (Refs. 99, 111). In CFBE41o− cells, treatment with lumacaftor/ivacaftor or tezacaftor/ivacaftor led to a significant reduction of EV release (Ref. 27). Although children with CF and healthy controls demonstrated equivalent EV counts, treatment with elexacaftor/tezacaftor/ivacaftor altered EV protein content in serum-derived EVs of patients with CF from different age groups (Ref. 110). Here, CFTR is linked to cystic fibrosis.