In the present study, we found that IL-27 was able to induce significantly higher expression of ICAM-1 and VCAM-1 and to augment TNF-α- and IL-1β-induced ICAM-1 and VCAM-1 on RA-FLS than that of control FLS (Figures 4 and 5), thus providing a novel immunopathological mechanism of IL-27 mediated joint inflammation in RA. The gene discussed is ICAM1; the disease is rheumatoid arthritis.