The observed association between claudin-14 and hypercalciuric nephrolithiasis [34] can be explained by claudin-14 deregulation that escapes microRNA suppression, inhibits claudin-16/-19 channel permeabilities and phenocopies FHHNC to variable degrees. This evidence concerns the gene CLDN14 and familial primary hypomagnesemia with hypercalciuria and nephrocalcinosis.