Given that NRF2 emerged as the only TF in our analysis that directly tracked both depression under basal conditions and the effects of antidepressant therapy, identification of the etiology of peripheral reactive oxygen species in MDD and its relationship to other immune-related transcriptional dynamics (for example, type I interferon signaling, NF-κB activity, CREB activity and so on) may provide deeper insights into the biological basis for depression. This evidence concerns the gene NFE2L2 and depressive symptom measurement.