This condition is characterized by rickets and the presence of large amounts of osteoid in bone (osteomalacia) and is accompanied by elevated circulating fibroblast growth factor 23 (FGF-23).(6–9) Using the Dmp1 null mouse as a model for human ARHR, we found that Dmp1 null osteocytes express elevated FGF-23, suggesting that Dmp1 might be a negative regulator of FGF-23 expression during bone development.(6). The gene discussed is FGF23; the disease is osteomalacia.