Indeed, the lower replication capacity 10-fold reduction of PIVCFTR compared to PIVGFP, in the context of >100-fold overexpression of CFTR in individual ciliated cells, suggests that further attenuation of PIV will continue to provide sufficient CFTR for correction of the CF MCT defect and possibly further reduce the generation of inflammatory mediators and cytotoxicity associated with our PIV vector prototype. This evidence concerns the gene CFTR and cystic fibrosis.