Although hyperphosphatemia, a typical serological feature of CKD patients, acts as an independent risk factor for cardiovascular death14,27, we are aware that altering phosphate homeostasis in vivo may lead to changes in FGF23, PTH, Klotho, and VitD, which can also contribute to myocardial hypertrophy and energy metabolism changes24,25. The gene discussed is PTH; the disease is cardiac hypertrophy.