Experimental studies have demonstrated that proinflammatory cytokines, particularly IL-6 and TNF-α, may contribute to depression pathogenesis through multiple mechanisms: (1) disrupting monoamine neurotransmitter synthesis and metabolism; (2) inducing structural and functional alterations in glutamatergic neurotransmission; and (3) impairing glucocorticoid receptor signaling [50–52]. Here, NR3C1 is linked to depressive symptom measurement.