Researchers identified PI3Kγ as a key component of CFTR macromolecular complex and uncovered a previously undescribed role for the kinase-independent function of PI3Kγ in the control of cAMP-mediated activation of CFTR. They showed a cell-permeable peptide targeting PI3Kγ scaffold function (Patent pending N° PCT/IB2015/059880) potentiates a localized pool of cAMP and, unlike the clinically advanced CFTR potentiator VX-770, stimulates chloride conductance of the most prevalent mutant CFTR, F508del, without interfering with the channel stability. They will optimize their peptide lead and explore the therapeutic potential of newly optimized and synthesized peptide derivatives in primary bronchial epithelial cells and in intestinal organoids from F508del patients.