The specific mechanism of RA is currently unknown, but many clinical phenotypes of RA have been reported, including inflammatory factors (such as tumor necrosis factor-α [TNF-α] and interleukin-8) in the joint environment of RA patients; these inflammatory factors lead to the vascular cell adhesion molecule-1 (VCAM-1) overexpression in the synovium around the joint. This evidence concerns the gene CXCL8 and rheumatoid arthritis.