The main sources of FGF23 are the osteoblasts and osteocytes in the skeleton [11], [28], [29], and a number of studies have shown that inactivating mutations in certain molecules expressed by these bone cells increase the plasma level of FGF23, which leads to hereditary hypophosphatemic rickets [10], [11], [13], [14]. This evidence concerns the gene FGF23 and Dent disease.