Released from the bone tissue in response to hyperphosphatemia, it acts both directly and indirectly: directly, through stimulating the mechanisms of fibrosis and myocardial hypertrophy after bonding to FGFR4 in cardiomyocytes in the presence of the alpha klotho coreceptor, and indirectly through hyperreninemia. This evidence concerns the gene FGFR4 and cardiac hypertrophy.