Given that NF‐κB activation promotes tumour progression, including cell proliferation, angiogenesis and metastasis, and that inhibiting NF‐κB can lead to tumour regression, our findings suggest that targeting TAB2 could enhance immunotherapy efficacy by reducing PD‐L1 expression and modulating the immunosuppressive microenvironment, making it a promising target, especially in combination with immune checkpoint inhibitors for CC treatment. The gene discussed is NFKB1; the disease is neoplasm.