Although it has not been reported for PI3K-related signaling in other studies about ginsenoside-treated osteoporosis, the PI3K/AKT pathway was considered to participate in anti-osteoporosis by promoting the proliferation of osteoblast precursors and the osteoblastic differentiation of BMSCs (bone marrow stromal cells), as well as autophagy and the differentiation of osteoclasts [20,29,30,31]. The gene discussed is AKT1; the disease is osteoporosis.