Clinical and animal studies have shown that potential therapeutic benefits of targeting FGF-23 include attenuating left ventricular hypertrophy, decreasing the synthesis of pro-inflammatory cytokines by the liver, improving neutrophil recruitment, rescuing anemia by stimulating erythropoiesis, and improving iron deficiency by down-regulating the synthesis of hepcidin. The gene discussed is FGF23; the disease is left ventricular hypertrophy.