Since the kidney is thought to be the primary regulator of circulating 1,25D levels (13, 29, 30), we hypothesized that kidney-specific Cyp24a1 deletion would replicate the phenotype of global deletion: increased serum 1,25D and vitamin D receptor (VDR) activation in all tissues, including the kidney and intestine, that results in hypercalcemia and suppressed PTH. The gene discussed is PTH; the disease is Hypercalcemia.