However, later studies in both humans and cats have shown that the increase in circulating intact FGF23 occurs independently of hyperphosphatemia and increased parathyroid hormone (PTH) in early CKD stages (Shimamura et al., 2012; Mace et al., 2015), suggesting that other stimuli must be involved in the upregulation of FGF23 secretion in CKD patients. The gene discussed is FGF23; the disease is chronic kidney disease.