CD8A and cancer: Obligate bsAbs create novel functions by (1) bridging cell types such as cytotoxic CD8+ T cells and cancer cells to induce T cell-mediated killing, (2) crosslinking receptors on cells to either inactivate or activate them, (3) positioning an enzyme and substrate as a cofactor mimetic, or 4) using one binding end to gain access into a restricted cellular compartment and using the other to exert a therapeutic effect, often referred to as “hijacking” or “piggybacking” [24].