This observation is particularly important, as the activation of innate immune mechanisms, especially proinflammatory cytokines Il-1, Il6 and tumor necrosis factor alpha (TNF-α), may contribute to the initiation and progression of mood disorders through their impact on the inter alia sympathetic system, hypothalamo–pituitary–adrenal axis and serotonergic pathways, leading to increased synthesis of catecholamines, glucocorticosteroids and synthesis of neurotoxic tryptophan metabolites [129]. The gene discussed is TNF; the disease is mood disorder.