CYP24A1 null mice that survive are unable to clear exogenously administered 1,25(OH)2D3.16 In humans, inactivating mutations in CYP24A1 have been reported to have a causal role in certain patients with idiopathic infantile hypercalcemia, providing further evidence for the role of CYP24A1 in 1,25(OH)2D3 catabolism.17 Elevated parathyroid hormone (PTH) resulting from hypocalcemia induces 1,25(OH)2D3 synthesis in the kidney and inhibits CYP24A1. This evidence concerns the gene PTH and Hypocalcemia.