Case 1 had normal total and ionized calcium and phosphorus concentrations, which is not typical for nutritional or known genetic rickets, including heritable renal phosphate wasting diseases, vitamin D-dependent rickets type I, hereditary vitamin D-resistant rickets, Cyp24al (24-hydroxylase) knockout, or calcium-sensing receptor knockout mice models [16]. This evidence concerns the gene CASR and X-linked dominant hypophosphatemic rickets.