Considering the decline in CYP27B1 and elevated CYP24A1 activity during CKD, preventing 1,25(OH)2D3 breakdown to improve the half-life of 1,25(OH)2D3 could offer a strategy that may improve vitamin D activity and possibly improve responsiveness to vitamin D therapies [20,21]. This evidence concerns the gene CYP24A1 and chronic kidney disease.