In CKD patients, FGF23 is highly upregulated leading to left ventricular hypertrophy by interaction with FGFR4, and subsequently stimulating hypertrophy-inducing cascades of PLCγ-calcineurin-nuclear factor of activated T-cells (NFAT) and Ras/MAPK, however, without the contribution of Klotho cofactor (Faul et al., 2011; Leifheit-Nestler et al., 2016). Here, FGF23 is linked to chronic kidney disease.