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. The gene discussed is KL; the disease is cardiac hypertrophy.