Utilization of the complement system offers potential for the elimination of tumor cells by monoclonal antibodies (mAb) immunotherapy. Activation of the complement system causes tumor cell destruction by inducing complement lysis and promoting cell ? mediated killing. In addition, complement can induce a strong inflammatory response, which might enhance other antitumor effector mechanisms. An important targets for mAb immunotherapy, however, are membrane bound complement regulatory glycoprotein: CD46, CD55 and CD59, which have been found to be expressed on most tumor cells in vivo and in vitro. Blocking or downregulation of these inhibitors could be an important step in the advancement of mAb immunotherapy.