STAT3 and neoplasm: Those results may indicate that special inflammatory mediators, TNFα, IL6, TGFβ, and complements, might create an immunosuppressive microenvironment with chronic inflammation in high-risk CC patients, which support tumour progression and metastasis by activating several signalling pathways, namely, NFκB, JAK-STAT3, TGFβ, and KRAS signalling.