The long-term survival of CD4+ T cells has been shown to affect the behavior of synovial fibroblasts through the cell-to-cell contact and the secretion of proinflammatory factors such as Th1 and Th17 cytokines [9,10], ultimately contributing to the maintenance and exacerbation of inflammation in RA [11]. The gene discussed is CD4; the disease is rheumatoid arthritis.