These findings are consistent with the studies by Jimi and Liu et al., who reported that sustained activation of NF‐κB not only promotes the overexpression of pro‐inflammatory cytokines such as TNF‐α, IL‐6, and IL‐1β, but also induces abnormal apoptosis in RA‐FLS cells. The gene discussed is NFKB1; the disease is rheumatoid arthritis.