In summary, this study unveiled the pivotal roles of key molecules (such as FTO/YTHDF1/ENST00000619282/Bax/Bcl-2) in the pathogenesis of RA, as well as the potential mechanism of XFC in inhibiting cell proliferation and apoptosis evasion by regulating these molecules and the NF-κB signaling pathway through a series of experiments (Figure 10). The gene discussed is FTO; the disease is rheumatoid arthritis.