The phosphaturic action of Fgf23 has been very well documented, and excessive circulating intact FGF23 actually leads to hypophosphatemia and rickets or osteomalacia.20, 21 Therefore, it is currently a conundrum why profoundly elevated serum levels of intact Fgf23 post‐MI do not translate into hypophosphatemia and hyperphosphaturia in the presence of unchanged serum PTH, the other major phosphaturic hormone. Here, PTH is linked to hypophosphatemia.