Traditionally, SHPT therapy revolved around maintaining normal calcium and phosphoruslevels and managing PTH levels with the help of calcium-based or non-calcium-basedphosphate binders, nutritional vitamin D supplementation, and active vitamin D (VDRactivation).2,4 However, these measures have limited effectfor a significant proportion of patients and have been associated with increasedrisk of hypercalcemia and hyperphosphatemia, which by their turn have been linkedwith increased mortality and cardiovascular disorders such as endothelialdysfunction and vascular calcification. The gene discussed is PTH; the disease is Hypercalcemia.