At present, as with cholesterol in the early 1960’s, associative but not causal evidence exists relating serum FGF-23 to cardiac disease in humans, and little is known about the distribution of serum FGF-23 levels in patients who might be especially responsive to a medication aimed at lowering or blocking the pathophysiologic effects of FGF-23, such as those with CKD or congestive heart failure (CHF). This evidence concerns the gene FGF23 and chronic kidney disease.