Klotho knockout mice, deficient for α-klotho, display a phenotype comparable with human ageing and are characterized by a mild hypercalcemia, hyperphosphatemia, increased levels of serum 1,25(OH)2D, decreased PTH and bone abnormalities such as increased metaphyseal trabecular bone mass and soft tissue calcifications, which are different from the phenotype caused by the translocation [hypophosphatemia, high PTH, and normal 1,25(OH)2D7] (87,88). Here, KL is linked to hyperphosphatemia.