Later on, it was shown that FGF23/FGFR4 signaling reversibly increases cardiac contractility and hypertrophy in vitro and in vivo and that an isoform-specific FGFR4 blocking antibody is reversing FGF23-mediated hypertrophic growth of isolated cardiac myocytes and established LVH in the animal model of CKD with high FGF23 levels [50]. This evidence concerns the gene FGF23 and chronic kidney disease.