These experimental data are supported by some clinical data fueling the hypothesis that FGF23 release and myocardial damage is not a one-way route from the skeleton to the myocardium: Cross-sectional data derived from a cohort study and post-hoc subgroup analyses from a randomized trial on mechanical assist device implantation support the hypothesis that the heart is an active player—not only a recipient—in FGF23 metabolism (70, 71): these patients had much higher FGF-23 than healthy individuals or patients with myocardial infarction not complicated by heart failure. The gene discussed is FGF23; the disease is myocardial infarction.