Specifically, 10− 6 M insulin induces insulin-resistance in human DPSCs, resulting in impairments in proximal insulin signaling events while maintaining the activity of distal pathway components, and continues to enhance the proliferation, osteogenic differentiation, and bone formation capability of human DPSCs via gradually attenuating the IIS/PI3K/AKT/mTOR pathway. This evidence concerns the gene AKT1 and Insulin resistance.