Experimental studies have suggested the direct cardiac effects of FGF23 and α-Klotho; for example, intramyocardial injection of FGF23 ameliorated the development of cardiac hypertrophy [7], and cardiac hypertrophy induced by certain pathologic conditions was found to be exaggerated in heterozygous Klotho-deficient mice and was lessened by either transfer of the klotho gene [14] or treatment with Klotho protein [15]. This evidence concerns the gene FGF23 and cardiac hypertrophy.