Castellani et al. [16] confirmed these previous results on TJ disorganization in CF cells by the lack of TJ proteins at cell-cell contacts (occludin, ZO-1, claudin 1, and JAM-1), and showed also that NHERF1 or CFTR overexpression in CFBE41o- cell (F508del homozygous) monolayers induced the reorganization of TJ proteins at the level of intercellular junctions and reduced the paracellular permeability to small solutes. Here, CFTR is linked to cystic fibrosis.