The observed PTH elevation can be mechanistically attributed to three principal factors: (1) hypocalcemia reduces activation of the calcium-sensing receptor (CaSR) on parathyroid chief cells, thereby relieving its tonic inhibition on PTH secretion (19–22); (2) acute hypocalcemia triggers rapid exocytosis of pre-synthesized PTH from secretory granules, elevating circulating PTH levels within minutes; and (3) sustained hypocalcemia promotes intracellular processing of PTH for storage and subsequent secretion. The gene discussed is CASR; the disease is Hypocalcemia.