In another prime example of how TME interactions can coordinate complex molecular pathways to protect tumor elimination by immune cells, the cell-cell contact-dependent interaction of bone marrow mesenchymal stromal cells (BMSCs) with multiple myeloma (MM) cells led to the upregulation of survivin (BIRC5), the anti-apoptotic capsase-3 inhibitor, rendering myeloma cells resistant to the cytotoxic machinery of T- and NK-cells [162]. Here, BIRC5 is linked to plasma cell myeloma.