However, in SLC34A2-intestinal-specific knockout mice, phosphatemia remains normal [27,28], and human inactivating mutations in SLC34A2 cause pulmonary alveolar microlithiasis, with an exclusive lung phenotype without hypophosphatemia [25] and without evidence of intestinal phosphate absorption alterations (Table 1). This evidence concerns the gene SLC34A2 and hypophosphatemia.