We previously reported that high FGF23 levels contribute to the development of anemia, iron deficiency, and inflammation, and that inhibition of FGF23 signaling or genetic deletion of Fgf23 results in increased erythropoiesis and serum iron levels, as well as amelioration of inflammation in mice with renal failure or normal kidney function [6,7,57]. The gene discussed is FGF23; the disease is acute kidney injury.