During early stages of CKD, alteration in mineral metabolism is marked by increasing FGF-23 and decreasing levels of co-receptor Klotho, which act in concert to induce renal phosphate excretion, suppress renal 1-alpha-hydroxylase activity, and inhibit PTH secretion in attempt to maintain phosphorus homeostasis (37–40). The gene discussed is PTH; the disease is chronic kidney disease.