THPT reflects the result of a long-standing SHPT in which the stimulated PGs are no longer in a reactive mode but have assumed a quasi-autonomous function, not too dissimilar from PHPT, with the emergence of a PTH-producing adenoma or rarely carcinoma [39,40] and the development of refractory HPT and hypercalcemia, in patients with previously normal serum calcium levels [29,39]. This evidence concerns the gene PTH and Hypercalcemia.