Despite its compensative role, an impact of FGF23 in CV events has recently been demonstrated both in the general population and in CKD using extrarenal actions: (a) the stimulation of liver inflammatory cytokines production, (b) the induction of cardiac myocytes hypertrophy, (c) the harmful modulation of the nitric oxide/oxygen-free radicals ratio causing endothelial dysfunction, atherosclerosis, and vascular calcification [6,7,8]. Here, FGF23 is linked to chronic kidney disease.