Generally, the bone involvement in MEN1 originates from multifactorial, intricate pathways, extending beyond the effects of MPHPT toward the co-diagnosis of PitNETs and GEP-NETs and their complications (e.g., persistent, endogenous hypercortisolism, diabetes or early hypogonadism, etc.)or to potential negative effects of menin itself on the bone metabolism [110,111,112]. The gene discussed is MEN1; the disease is adrenal gland hyperfunction.