Following successful KTx, patients regain functions of klotho via FGF23-Klotho signaling, and with the previously accumulated FGF23, residual hyperparathyroidism, and the use of calcineurin inhibitors (especially cyclosporine) [93,94,95], post-KTx hypophosphatemia can commonly occur up to 86% [85,96,97]. This evidence concerns the gene FGF23 and hypophosphatemia.