For example, complete resection of FGF23-producing tumours has resolved hypophosphatemia, osteomalacia, bone pain and improved other skeletal manifestations in TIO [128, 129] and administration of FGF23-blocking antibodies has improved growth retardation of juvenile Hyp mice, accelerating weight gain, increasing tail length, decreasing osteoid volume and thus improving bone mineralisation while improving elongation of femoral and tibial bones [130–132]. The gene discussed is FGF23; the disease is hypophosphatemia.