Mutations in fibroblast growth factor 23 (FGF23) and PHEX account for approximately 60% of hypophosphatemic rickets with eucalciuria and are associated with abnormalities in dentin and bone.(1) Mutations in the type 2a sodium-phosphate cotransporter lead to hereditary hypophosphatemic rickets with hypercalciuria (HHRH).(2–6) The molecular defects responsible for the remaining hypophosphatemic patients are unknown. Here, FGF23 is linked to hereditary hypophosphatemic rickets with hypercalciuria.