In fact, in genetic mice models, either suppressing FSHR (FSHR−/− mice) or its ligand (FSHβ−/− m ice), osteoclastogenic activity did not result in bone loss compared to eugonadal controls (FSHR+/+ and FSHβ+/+ mice), despite severe hypogonadism, while bone mineral density (BMD) decreased in ovariectomized mice. The gene discussed is FSHR; the disease is hypogonadism.