In the context of cancer, sustained NF‐κB activation drives persistent ICAM‐1 expression, promoting tumor cell adhesion and metastasis.[33, 34, 35] In this study, we demonstrate that ICAM1 acts as a key mediator of exosomal CMTM4‐induced M2 polarization and NF‐κB activation, both of which significantly contribute to OC progression and metastasis. This evidence concerns the gene NFKB1 and neoplasm.