A recent series of in vivo and in vitro experiments demonstrated that the effects of inflammation and iron deficiency on FGF23 is mediated through HIF-1α; and induction of functional iron deficiency by administration of exogenous hepcidin increased osseous FGF23 mRNA expression and serum levels of inactive c-terminal FGF23 (cFGF23), whereas concentrations of the intact molecule (iFGF23) were unaffected [7]. The gene discussed is HIF1A; the disease is Iron deficiency anemia.