In agreement with previous reports [39], mRNAs of Cldn16 (Fig. 3o) and Cldn19 (Fig. 3p), both responsible for familial hypomagnesemia with hypercalciuria and nephrocalcinosis [7, 73], were mostly restricted to kidney, though Cldn16 immunoreactivity has been reported at the basal membrane of acinar cells in human submandibular glands [45]. This evidence concerns the gene CLDN19 and familial primary hypomagnesemia.