Notably, their study uncovered diminished soluble Klotho in CKD patients' myocardial tissue, displaying a negative correlation with LVH, while FGF23 demonstrates the capability to activate FGFR4 irrespective of soluble Klotho presence, as demonstrated in cultured cardiomyocytes, where FGF23-induced hypertrophy was inhibited by an FGFR4-specific blocking antibody [6]. Here, FGFR4 is linked to chronic kidney disease.