Although the authors of previous studies have reported the systemic metabolic improvement of DM rat models after receiving glabridin [16,17], our in vitro results provide evidence to support the direct effect of glabridin on preosteoblast cells under oxidative stress conditions via the Akt/NF-κB and Akt/GSK-3β signaling pathways, leading to cell proliferation stimulation and apoptosis prevention. The gene discussed is GSK3B; the disease is diabetes mellitus.