The evidence of SLC26A9′s role as a gene modifier and of its coexpression with CFTR in several organs involved in CF suggests that therapeutic strategies increasing the level and/or function of SLC26A9 could represent an alternative method to bypass the defect of ion transport [117], which would be useful not only as therapy in CF but also for the treatment and prevention of CFRD [117]. This evidence concerns the gene CFTR and cystic fibrosis-related diabetes.