Hepcidin overexpression attenuated OP processes in mice, implying that hepcidin could be a prospective drug target for preventing postmenopausal osteoporosis.[125] Furthermore, the overexpression of divalent metal transporter 1 (DMT‐1) in osteoblasts induced autophagy and apoptosis in osteoblasts, thus promoting OP, by inducing cellular iron overload.[126]. This evidence concerns the gene HAMP and postmenopausal osteoporosis.