Although the aforementioned short‐term EPO and FG‐4592 in vitro and in vivo studies caused FGF23 increases in normal animals and cells, the reduction of circulating FGF23 by improving iron utilization in CKD supports that suppression of FGF23 over the long term is a stronger effect than the acute stimulatory ability of ESAs on FGF23 synthesis. The gene discussed is EPO; the disease is chronic kidney disease.