It has been shown that FSH enhances osteoclastogenesis by activating MEK/Erk, NF-κB, and Akt; furthermore, FSHβ KO mice and FSH receptor (FSHR) KO mice are resistant to bone loss despite severe hypogonadism; FSHβ+/− mice exhibit increased bone mass and decreased osteoclastic resorption with normal ovarian function, suggesting that the skeletal action of FSH is estrogen independent [84]. Here, BRD2 is linked to hypogonadism.