Despite the biological plausibility of an association between elevated pre-transplant PTH levels and graft dysfunction—via mechanisms such as hypercalcemia-induced vasoconstriction, tubulointerstitial calcification, and phosphate imbalance—our results did not support this link.(24,25) One possible explanation is that post-transplant management, including the use of vitamin D analogs, phosphate binders, and cinacalcet, may mitigate the potential adverse effects of preexisting hyperparathyroidism, resulting in improved metabolic control and reduced complications.(26). The gene discussed is PTH; the disease is Hypercalcemia.