Isoforms of caveolin-2 might rescue mis-folded CFTR proteins (e.g., F508del-CFTR) resulting in increased cell surface expression of mutant CFTR and improved lung defenses against P. aeruginosa. While the mechanism(s) by which CAV2 rs8940 influences risk of chronic P. aeruginosa airway infection in persons with CF remains to be determined, our results are consistent with the known functional roles of caveolins in response to P. aeruginosa infection in CF models and highlight caveolin-2 as a potential therapeutic target to block P. aeruginosa invasion. This evidence concerns the gene CFTR and cystic fibrosis.