In the present study, we inhibited MBTP1 and thus the cleavage and activation of ATF6 to alleviate p.Phe508del-CFTR defects, in a non-transduced Human Bronchial Cell line and in bronchial epithelia from patients, to be as close as possible to the physiopathology of CF in a relevant cell model. This evidence concerns the gene ATF6 and cystic fibrosis.