In addition, changes in the potentialdifference on the epithelial cell membrane in nasal airways were recorded,which was an indication of the restoration of the normal phenotype in micecarrying the most common CF mutation, ΔF508[54].The problem of the limited size of the genetic constructpacked in AAV2 may be solved by developing a short synthetic promoter[55] or obtaining a CFTR genewith partial deletion of the regulatory domain[56]. This evidence concerns the gene CFTR and cystic fibrosis.