For instance, NCOA3 upregulation leads to the suppression of inflammatory responses in postoperative ileus while aggravation of inflammation in rheumatoid arthritis.24 Through a series of experiments, our results showed that IGF2BP2 upregulation increased the m6A levels of NCOA3 as well as the mRNA level and mRNA half-life period of NCOA3, suggesting that IGF2BP2 may recognize and bind to the m6A site of NCOA3 and then increase the mRNA stability of NCOA3. The gene discussed is NCOA3; the disease is rheumatoid arthritis.