The role of inflammation in the pathogenesis of depression is supported by studies showing increased levels of proinflammatory cytokines, such as IL-1β, IL-6, IL-12, TNF-α, and prostaglandin E2 (PGE2), in patients with depression (26, 27), and by some experiments in preclinical models in which the administration of inflammatory cytokines promoted a depressive-like syndrome (28, 29). This evidence concerns the gene IL1B and major depressive disorder.