KRAS and neoplasm: 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).