We postulated the existence of a Klotho-independent signaling pathway of FGF23 in the parathyroids based on the findings that PTH-KL−/− mice had unaltered serum PTH levels, a intact parathyroid response to FGF23 injections and that hyperparathyroidism was not aggravated in the setting of renal failure despite an effective ablation of parathyroid Klotho and an apparent lack of MAPK activation in response to FGF23. The gene discussed is PTH; the disease is acute kidney injury.