KDM6B and postmenopausal osteoporosis: As bone remodeling involves a complex interplay among the immune system, osteoblasts, and osteoclasts, estrogen deficiency has been shown to be linked with increased inflammation, enhanced osteoclast differentiation and decreased osteoblast activity.1 As such, the examination of KDM6B’s interaction with inflammatory processes such as NF-κB signaling and the osteoblast apoptotic pathway may reveal KDM6B’s role as a main epigenetic player in estrogen-mediated bone homeostasis and its potential to guard against postmenopausal osteoporosis.