Collectively, our results suggest that GTE precludes excessive bone loss due to postmenopausal osteoporosis by inducing bone formation through Bmp2-Smads 1/5/8-Runx2 signaling and interrupts osteoclastogenesis via RANKL/OPG binding and lowered Nox-4 activity (Figure 6E). The gene discussed is NOX4; the disease is postmenopausal osteoporosis.