The PVN of the hypothalamus is crucial in regulating sympathetic outflow for bone homeostasis.11 Excessive activation of GR or insufficient activation of MR promotes neuronal apoptosis and dendritic atrophy, which lead to cognitive, emotional and neuroendocrine disorders.22 GR and MR interact and even form heterodimers, they may function in complementary or opposite ways depending on the microenvironment.56,57 MR contributes to maintaining the physiological sympathetic activities.58 Our results firstly showed that an imbalance in GR and MR activation occurred in mice with GC-treated ONFH. The gene discussed is NR3C1; the disease is neuroendocrine disorder.