FGF23 and X-linked dominant hypophosphatemic rickets: Patients with XLHR present with elevated FGF23 levels, which is currently considered to be an important phosphorus‐regulating factor involved in a bone–kidney axis regulating phosphate homeostasis and matrix mineralization.[5, 6, 7, 8] However, the role of FGF23 in the pathophysiology of XLHR is incompletely understood.