However, FGF23 has a putative role in promoting cardiac fibrosis and left ventricular hypertrophy, as shown in animal and human studies, via FGFR-dependent activation of the calcineurin–NFAT pathway; this mechanism appears to be independent by the presence of klotho, which is necessary for FGF23 in exerting its role in parathyroid glands and kidneys [177,178]. This evidence concerns the gene FGF23 and left ventricular hypertrophy.