Increased pro-inflammatory cytokine expression in the brain, especially tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in the hippocampus, amygdala, anterior cingulate, and frontal cortex, contributes to the development of depression pain comorbidity, which has been repeatedly shown in rodent models of neuropathic and inflammatory pain that also exhibit depressive-like behavior and, conversely, in rodent models of depression that also display altered nociceptive responses [11–13]. Here, IL1B is linked to depressive symptom measurement.