Cystic fibrosis (CF) is a genetic disease caused by the mutation of the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) gene and results in a decreased Cl- secretion and hyperabsorption of Na+ in the airway leading to dehydration of the Airway Surface Liquid (ASL) layer. The reduction in ASL height impairs mucocillary clearance and favours chronic bacterial infection, sustained inflammation and progressive lung destruction. The eicosanoid lipoxin A4 (LXA4) which is inadequately produced in the lungs of patients with CF, is described as a signal for resolution of inflammation. In addition, LXA4 regulates several airway epithelial function. LXA4 stimulates Cl- secretion (1) resulting in an increase of ASL height in Human Bronchial Epithelial (HBE) and Cystic Fibrosis Bronchial Epithelial (CFBE) cells (2). Consistent with a role in resolution of inflammation, LXA4 regulates the epithelial structure and enhances airway epithelial barrier integrity. LXA4 stimulates ZO-1 expression and increases transepithelial electrical resistance (3). LXA4 stimulates airway epithelial cell migration, proliferation and wound repair through the activation of KATP potassium channels and ERK signalling pathway (4). Taken together, these results highlight novel roles for LXA4 in airway epithelial physiology which may lead to new therapeutic routes for patients with CF.