On the contrary, Larsson et al. [20] generated transgenic mice overexpressing human FGF-23 and found that FGF-23 transgenic mice recapitulated the biochemical and skeletal abnormalities similar to human autosomal dominant hypophosphatemic rickets, oncogenic osteomalacia and X-linked hypophosphatemia. The gene discussed is FGF23; the disease is osteomalacia.