Although whether the Ca2+-dependent activation of chloride channels in CF bronchial epithelial cells could partially vary the defects of CFTR ion transport is presently under scrutiny (173), the results recalled above support the concept that the up-regulation of intracellular Ca2+ signaling is a key amplifier of the inflammatory response and lung pathogenesis in CF, which opens the issue of new potential molecular therapeutic targets. This evidence concerns the gene CFTR and cystic fibrosis.