The results of this study show that: (1) METTL3 is upregulated obviously in human RA synovial tissues and rat AIA synovial tissues; (2) METTL3-RNAi inhibited the expression of pro-inflammatory factors in RA-FLSs and AIA-FLSs, as well as the proliferation, invasion, and migration of these cells; (3) in RA-FLSs and AIA-FLSs, METTL3 overexpression promoted pro-inflammatory cytokine expression, proliferation, invasion, and migration; and (4) METTL3 expression may be closely related to the NF-κB signaling pathway. This evidence concerns the gene METTL3 and rheumatoid arthritis.