CLCN5 and Hypercalciuria: The hypothesis that hypercalciuria in mice with defective ClC‐5 function is in fact due to intestinal hyperabsorption of calcium rather than a renal leak was supported by another ClC‐5 KO mouse model.52 By targeting ClC‐5 expression with antisense ribozyme, the authors demonstrated that hypercalciuria was abolished by calcium deprivation, suggesting that intestinal calcium hyperabsorption was important.