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. Here, NFKB1 is linked to cervical carcinoma.