Our findings revealed that DBD intervention effectively blocked the excessive activation of the NF‐κB signaling pathway, primarily by significantly reducing the phosphorylation levels of key pathway proteins in synovial tissues and RA‐FLS cells, such as p‐IκBα, p‐p65, and p‐IKKα, as well as by inhibiting the overactivation of the NLRP3 inflammasome. The gene discussed is NFKB1; the disease is rheumatoid arthritis.