Comorbid TLE and depression associated with dysfunction of the HPA axis are based on common molecular and cellular mechanisms, including the dysfunction of glucocorticoid receptors, neurotransmitters, and neurotrophic factors, and the development of neuroinflammation, leading to neurodegeneration and loss of hippocampal neurons, as well as disturbances in neurogenesis in the subgranular neurogenic niche and formation of aberrant neural networks [58]. Here, NR3C1 is linked to depressive symptom measurement.