Together, these results suggest that i) B49Mod1 inhibits adhesion of BST-2-expressing and BST-2-suppressed cancer cells but not immune cells to ECM substrates, ii) immune cells whether incoming or resident are not responsive to B49Mod1-mediated inhibition of adhesion, and iii) monolayer cells treated with B49Mod1 may not provide a permissive niche for incoming BST-2-expressing tumor or immune cells. Here, BST2 is linked to neoplasm.