In autoimmune diseases, although the overexpression of METTL3 has been shown to attenuate the inflammatory response induced by LPS in macrophages dependent on NF-κB to influence rheumatoid arthritis (RA) progression [114], the effect of METTL3 on systemic lupus erythaematosus (SLE) remains a matter of speculation [115]. The gene discussed is NFKB1; the disease is rheumatoid arthritis.