These results mirror our observations in a previous study on cardiac remodeling in the 5/6 nephrectomy rat model of CKD in which inhibition of the FGF23–FGFR4–calcineurin–nuclear factor of activated T cells signaling pathway prevented cardiac remodeling without altering serum phosphate levels.13,15,16,27 Taken together, these findings argue against a major FGF23-independent role of phosphate in driving heart failure in CKD, but further studies are warranted to explore potentially toxic interactions between elevated phosphate and FGF23, as occurs in CKD. The gene discussed is FGFR4; the disease is chronic kidney disease.