Experimental studies and clinical studies in patients with chronic kidney disease (CKD) and the general population have shown that FGF23 induces left ventricular hypertrophy by activating the PLCγ/calcineurin/NFAT pathway via FGF receptor 4 independent of the co-receptor α-Klotho [10, 11] and causes arterial stiffness via enhanced FGF receptor-dependent reactive oxygen species (ROS) production [12, 13]. This evidence concerns the gene FGF23 and chronic kidney disease.