However, co-potentiation with ivacaftor / ASP-11 restored therapeutically relevant levels of channel activity to N1303K-CFTR homozygous primary nasal epithelial cells (i.e. the magnitude of the potentiated short-circuit current was equivalent to that achieved in CF airway epithelial cells (genotype F508del/F508del) after correction with lumacaftor and potentiation by ivacaftor) [74,76]. Here, CFTR is linked to cystic fibrosis.