There is emerging evidence that non-receptor tyrosine kinase BMX is involved in the pathogenesis of inflammatory disorders, such as rheumatoid arthritis (RA).[7,20,21] An siRNA against BMX-inhibited lipopolysaccharide (LPS)-induced IL-6 secretion in synovial fibroblasts.[22] In macrophages and synovial fibroblasts from RA patients, overexpression of BMX mediates an increase in LPS-induced stabilization of the IL-6 mRNA.[20,21] In the absence of LPS, overexpression of BMX failed to induce IL-6 mRNA expression. The gene discussed is BMX; the disease is rheumatoid arthritis.