Taken together, our findings reveal a multifactorial interplay in cervical cancer progression, in which viral oncogenesis (via HPV), immune signaling (STAT3/NF‐κB), cellular players (M2‐TAMs, Tregs), and host genetic background (FOXP3 and HLA‐G polymorphisms) operate in concert to drive immune escape and worsen clinical outcomes. This evidence concerns the gene NFKB1 and cervical cancer.