Hypercalcemia in sarcoidosis is attributed to 3 potential mechanisms: (1) systemic extrarenal conversion of 25(OH)D to 1,25(OH)2D by 1α-hydroxylase produced by granulomatous macrophages and the consequential increase in intestinal calcium absorption; (2) granuloma production of PTHrP causing increased renal calcium absorption and bone resorption, similar to humoral hypercalcemia of malignancy; and (3) tissue-level conversion of 25(OH)D to 1,25(OH)2D by local granulomatous macrophages [9]. Here, PTHLH is linked to hypercalcemia disease.