These activated RA-FLSs accelerate joint damage through multiple pathways: releasing inflammatory cytokines (e.g., TNF-α, IL-1, IL-6), secreting matrix metalloproteinases to degrade cartilage, and directly eroding bone tissue via osteoclast differentiation regulation (Singh et al., 2023; Yoshitomi, 2019). The gene discussed is TNF; the disease is rheumatoid arthritis.