Since chronic stress exposure is a pathological stimulation, we hypothesize that 35-day CUS stimulation may disrupt the homeostasis of some targets that mediate the production of pro-inflammatory cytokines and the progression of oxidative and nitrosative stress, such as nuclear factor-kappa B (NF-κB) and nuclear factor erythroid-derived 2-like 2 (Nrf2), thereby promoting the development of depression-like behaviors. The gene discussed is NFKB1; the disease is depressive symptom measurement.