Increased mRNA expressions of FGF23 in the bone, bone marrow, and renal tissues are found in several AKI mouse models.384–386 This could be reversed by pretreatment with PD173074, an FGFR inhibitor, or blocking the erythropoietin receptor.384,386 These results indicate that the increased circulating erythropoietin and erythropoietin receptor activation are involved in the mechanisms leading to increased plasma FGF23 in AKI. The gene discussed is EPOR; the disease is acute kidney injury.