These findings also underscore the significance of macrophages in promoting RA-derived FLS (RA-FLS) proliferation and secretion of inflammatory mediators, including interleukin 1β (IL-1β), interleukin 6 (IL-6), interleukin 8 (IL-8), and tumor necrosis factor α (TNF-α), ultimately contributing to synovial hyperplasia, cartilage and bone erosion, joint inflammation and stiffness [7–9]. The gene discussed is IL6; the disease is rheumatoid arthritis.