Even though inflammatory cytokines alterations are not specific to depression, there is also evidence that they are overexpressed in dysthymic disorders, such as generalized anxiety and depression, and IL-1β is the main mediator in the acute phase [26]; while prolonged stress causes activation of a series of receptors, such as monoaminergic, glutamate, and neuropeptide systems, and decreases in growth factors, such as brain-derived neurotrophic factor, which in turn also activate the transcription factors NF-kB and TNFα, increasing levels of IL-1β and IL-6, among others [27]. Here, NFKB1 is linked to depressive symptom measurement.