Therefore, to further elucidate how CFTR dysfunction triggers EMT in CF we investigated the ability of two CFTR variants, each characterized by distinct molecular defects, to promote EMT: p.Phe508del (class II), which is retained in the endoplasmic reticulum and does not reach the PM, and p.Gly551Asp (class III), which reaches the PM but lacks ion channel function. This evidence concerns the gene CFTR and cystic fibrosis.