The mechanisms potentially involve TNF‐α/NF‐κB‐mediated immune microenvironment remodelling, KRAS‐driven MAPK/ERK pro‐proliferative cascades and sustained IL‐6/JAK/STAT3 pathway activation synergistically inducing key EMT‐related transcription factors, while potentially augmenting tumour cell migratory capacity, invasive potential and distant metastasis predisposition through up‐regulated immune checkpoint molecules (e.g., PD‐L1). The gene discussed is NFKB1; the disease is neoplasm.