Our results suggested that a major component of the anti-B7-1 expressing tumor immunity is T effectors but not NK effectors because: 1) the RMA-S/B7-1 tumors grew quickly in PBS-immunized mice while no RMA-S/B7-1 tumors appeared in tumor-immunized mice at initial week and 2) NK activity could only inhibit less than 1×106 challenged B7-1 expressing RMA-S cells per mouse [22]. This evidence concerns the gene CD80 and neoplasm.