Among the common cervical cancers in women worldwide, human papillomavirus (HPV) infection is the most significant factor, and HPV 16 and 18 evade antiviral effects by reducing downstream activation of the NF‐κB and IFN signaling pathways of TLRs through the E6/7 protein and promoting tumor development [125]. This evidence concerns the gene NFKB1 and neoplasm.