Using a combination of sedimentation analysis coupled with TEM, we identified changes in mucin forms after Tmem16a loss that are consistent with impaired MucXS expansion/remodelling post-secretion, comparable to those observed for mucins in cystic fibrosis mucus and in vivo and in vitro under conditions that inhibited Cl−and bicarbonate secretion68. This evidence concerns the gene MUC5AC and cystic fibrosis.