Theories have included the pulsatile secretion of PTH, the secretion of abnormal PTH altering its measurement but not its function, the presence of unmeasured active PTH fragments, the presence of a circulating antibodies interfering with the assay, the presence of another mediator of hypercalcemia (PTH-related peptide), and the increased peripheral tissue sensitivity to normal PTH [2, 8, 10, 14, 16, 17, 25]. This evidence concerns the gene PTH and hypercalcemia disease.