Its role in the setting of cardiomyocyte FGF23 toxicity thus remains controversial: While Faul reported a Klotho-independent effect of FGF-23 on cardiomyocytes, other groups suggested that klotho deficiency rather than a FGF23 excess causes cardiac hypertrophy (63): In heterozygous klotho-deficient CKD mice, the development of LVH was not modified by interventions normalizing FGF23 and phosphate levels, but only via exogenous klotho application. Here, FGF23 is linked to chronic kidney disease.