Pharmacological blockade of FGF-23 or Ang II will be need to tease out the indirect effects of FGF-23 from those mediated by Ang II activation of angiotensin receptors78.The clinical importance of cross talk between RAAS and FGF-23, however, is suggested by the finding that FGF-23 levels are higher in patients with heart failure not treated with angiotensin converting enzyme inhibitors (ACEi) and patients in the top tertile of elevated serum FGF-23 exhibit a lower risk of adverse events after treatment with ACEi79. This evidence concerns the gene FGF23 and heart failure.