Also, there are studies suggesting that FGF23 increases PTH secretion and gene expression in in vivo animal models, the PTH levels in CKD patients may be increased in response to hypocalcemia due to suppressed 1,25(OH)2D3 and may be explained by hyperplasia in parathyroid as a result of secondary hyperparathyroidism to maintain the Ca levels by Casensitive receptors [18], [19]. This evidence concerns the gene FGF23 and secondary hyperparathyroidism.