Recent studies indicate that factors other than monoamine deficiency or hyperactivation of the HPA axis must be considered when examining the pathogenesis of major depression such as an altered activation of immune system and chronic inflammation with a specific impairment in the signaling of neurotrophins, such as transforming growth factor β1 (TGF-β1) [124, 125]. This evidence concerns the gene TGFB1 and major depressive disorder.