Initially, FGF-23 is reported to be implicated in the regulation of phosphatemia and mineral metabolism via interacting with its co-receptor klotho in kidney, and growing recent clinical evidences demonstrate the regulatory role of FGF-23 in diverse pathological processes of cardiovascular diseases (such as: coronary artery stenosis, myocardial fibrosis, cardiac injury, atherosclerosis, vascular calcification) and potential of FGF-23 as a clinical biomarker for predicting higher risk of adverse cardiovascular outcomes [8–10]. This evidence concerns the gene FGF23 and atherosclerosis.