Interestingly, data are available on rheumatoid arthritis (RA), where previous studies reported that Fos/AP-1 and interleukin 1β (IL-1β) influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that, in turn, seems to have an important role in the accrual of joint damage in experimental RA models characterized by the enhancement of Fos/AP-1 activity. The gene discussed is IL1B; the disease is rheumatoid arthritis.