Because TTP protein domains are remarkably conserved within vertebrates, and share a common regulatory mechanism [33, 34], we made use of fibroblasts derived from wild-type (ZFP36+/+) and TTP knockout (ZFP36−/−) mice [35], and stimulated them with IL-1β to mimic experimental conditions used in RA FLS. The gene discussed is IL1B; the disease is rheumatoid arthritis.