However, major pathogenetic mechanisms underlying BD are linked to innate immune cell activation and dysregulation, and hyperactivity of neutrophils, T-helper- (Th-) 1, and Th-17 natural killer (NK) cells, the main result of which is the critical overproduction of proinflammatory cytokines, such as tumor necrosis factor- (TNF-) α, interleukin- (IL-) 1β, IL-6, and IL-17 [10]. This evidence concerns the gene IL6 and Behcet disease.