GS is characterized by chronic hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria.[1,2] Patients with GS typically do not present with hypercalcemia due to hypomagnesemia-induced parathyroid hormone (PTH) secretion dysfunction and end-organ resistance.[3–7] Primary hyperparathyroidism (PHPT) is typically characterized by hypercalcemia associated with inappropriately elevated PTH levels.[8] Therefore, in instances where hypercalcemia emerges in GS, consideration of PHPT is warranted. This evidence concerns the gene PTH and primary hyperparathyroidism.