And contrary to previous opinions (64), they also found that long-term exposure to TNF, which was considered to be an important cytokine in the pathogenesis and development of RA, could protect RA-FLSs from ferroptosis by promoting cystine uptake and GSH synthesis, while IL-6 and transforming growth factor-β (TGF-β) could increase the sensitivity of FLSs to ferroptosis (39). The gene discussed is TNF; the disease is rheumatoid arthritis.