While transgenic mice overexpressing FGF23 have phenotypes similar to the clinical characteristics of XLH, mice with deletions in FGF23 show hyperphosphatemia, ectopic mineralization and poorly formed skeletons with extremely low PTH levels; they also show increased 1,25(OH)2 vitamin D3, which suppresses PTH levels attenuating an increase in circulating FGF23 [38]. Here, PTH is linked to X-linked dominant hypophosphatemic rickets.