Mutations in tumor suppressor genes such as p53, and elevated expression of proto-oncogenes and apoptosis inhibitors, such as c-myc, c-fos, c-ras, c-jun, and bcl-2 in RA synoviocytes, may lead to inadequate apoptosis and tumor-like proliferation of rheumatoid synoviocytes [8-11]. The gene discussed is JUN; the disease is neoplasm.