John R et al. observed with fluorescence confocal microscopy that the biotinylated DNA aptamer of MUC1-5TR-1 can modify the plasma membrane of human breast cancer (MCF7) cells, initiating the classical complement pathway, leading to the anchoring of complement on target cells through streptavidin–C1q complexes that synergistically target different surface-bound tumor markers of the aptamer–C1q complex mixture, which can inhibit CRP on MCF7 cells and provide antitumor efficacy [111]. The gene discussed is CRP; the disease is neoplasm.