The etiology of BD remains unclear, but previous studies on the circulating CD4+ T cells and affected lesions of BD patients with active disease showed elevated levels of T-helper 1 (Th1) cytokines, such as IFNγ and IL-12, indicating that a Th1-polarized immune response plays a major role in the pathogenic process [2-4]. This evidence concerns the gene CD4 and Behcet disease.