It is also not surprising that impairments in the phosphaturic FGF23-klotho system lead to hyperphosphatemia, as shown in genetic mouse models that lack FGF23 (Fgf23−/−) or klotho (kl/kl), which both develop severe ectopic calcifications in the absence of kidney injury [102–105]. The gene discussed is KL; the disease is hyperphosphatemia.