To verify whether the promoting effects of IgG on LPS-induced proinflammatory cytokine production were due to the increase of TLR4 expression in cervical cancer cells, we upregulated or downregulated TLR4 expression in HeLa cells stably expressing IGHG1 shRNA or control shRNA and activated the signaling pathway by LPS stimulation. The gene discussed is IGHG1; the disease is cervical carcinoma.