Risk factors include pre-existing CKD-MBD and renal osteodystrophy, immunosuppressive therapies including not only corticosteroids but also calcineurin inhibitors and mTor inhibitors, reduced graft function, metabolic acidosis, malnutrition, hypogonadism, reduced physical activity, as well as disruption of the phosphocalcic axis (i.e., parathyroid hormone (PTH), 25-hydroxyvitamin D, and fibroblast growth factor 23 (FGF23) axis), leading to persistently elevated FGF23 and PTH levels for weeks/months post-KTx that further induce hypophosphatemia and subsequent mineralization defects [6–8]. The gene discussed is PTH; the disease is hypogonadism.