The establishment of X-linked hypophosphatemia (XLH) mouse models, characterized by elevated serum FGF23 levels, which caused decreased 1,25(OH)2D3 levels and hypophosphatemia, led to the discovery of the role played by phosphate in osteocyte functioning, which is triggered in response to disruption of plasma phosphate homeostasis.103 How osteocytes sense phosphate levels and subsequently regulate perilacunar remodeling103 and FGF23 and 1,25(OH)2D3 synthesis104 is still unclear. The gene discussed is FGF23; the disease is hypophosphatemia.