It can exert many biological activities such as the possible link to depression by reducing pro-inflammatory mediators tumor necrosis factor alpha (TNF-α), Interleukin- 1β (IL-1β), Interleukin-6 (IL-6), and interferon-c (IFNc), probably via the Jun N-terminal kinase (JNK1/2) and p 38 mitogen-activated protein kinases (p 38 MAPK) signaling pathway [29]. This evidence concerns the gene IL1B and depressive disorder.