These ligand-receptor pairs suggest a potential immune evasion mechanism: sustained antigen exposure may collectively foster an immunosuppressive microenvironment in both extracranial and brain metastases, while within MBMs, MBMATCs may directly interact with and potentially suppress exhausted T cells through FN1/LAMA4 secretion, concurrently remodeling the brain niche to facilitate tumor cell colonization. This evidence concerns the gene FN1 and neoplasm.