In conclusion, we have demonstrated that during the pseudoglandular stage of lung development fetal hypercalcemia of a magnitude similar to that seen physiologically in the prenatal period activates the CaSR leads to an increase in Ca2+i, which in turn activates the Ca2+-stimulated AC1, inducing opening of CFTR within the apical membrane of the developing pulmonary epithelium (Fig. 5). The gene discussed is CFTR; the disease is hypercalcemia disease.