Because the etiology of depression is increasingly recognized as immune activation through secretion of proinflammatory cytokines, such as IL-1, IL-6, TNF-α, IFN-γ, leukotrienes, and prostaglandins, anti-neuroinflammatory activity has been proposed by many as a potential treatment for depression [33, 34]. The gene discussed is IFNG; the disease is major depressive disorder.