Based on the above findings, we hypothesised that signalling between LFA-1 on tumour cells and ICAM-1, or its alternative ligands ICAM-2, ICAM-3, ICAM-4 and junctional adhesion molecule-1 (JAM-1) [14, 15], contribute to successful tumour growth within the brain parenchyma, and that molecules within the LFA-1 signalling pathways may provide potential therapeutic targets in brain metastasis. This evidence concerns the gene F11R and neoplasm.