The idea of bone is an endocrine organ that secretes FGF23 to coordinate renal phosphate handling to match bone mineralization and turnover has arisen from the studies of X-linked hypophosphatemia (XLH) and autosomal recessive hypophosphatemic rickets (ARHR).(4,6–9) XLH and ARHR have similar phenotypes, characterized by elevated FGF23 levels, hypophosphatemia, aberrant regulation of 1,25(OH)2D production, and rickets/osteomalacia. This evidence concerns the gene FGF23 and X-linked hypophosphatemia.