Just to name a few, the community needs to prove how cardiac disease induces (rather than follows) FGF-23 secretion, to what degree cardiomyocytes may themselves produce FGF-23 in health and disease, whether such locally produced FGF-23 has a physiological role in (acute) myocardial damage; and whether or not (systemic) FGF23 excess itself directly drives the development of myocardial damage. This evidence concerns the gene FGF23 and heart disorder.