In this setting, monotherapy with extended-release calcifediol achieves dose-dependent increases of 25(OH)D and physiological increases in 1,25(OH)2D, with sustained reduction of parathyroid hormone levels, comparable to what can be achieved with active vitamin D analogues; however, extended-release calcifediol does so with less risk of hypercalcaemia and has the added benefit of also replenishing 25(OH)D. This evidence concerns the gene PTH and Hypercalcemia.