CD8A and neoplasm: Collectively, these findings suggest a model wherein hIgG1-G396R fuels immune responses against tumors in at least 4 ways: (a) elevated tumor-specific IgG1 production, which promotes avidity of macrophages, DCs, and NK cells toward IgG1-bound tumors (56, 57); (b) improved ADCP by macrophages and DCs; (c) enhanced presentation of TAAs and neoantigens to potentiate CD8+ T cell activation; and (d) potentiated formation of functional TLSs, in which switched memory B cells are enriched in responders and synergize with killer T cells for effective tumor cell targeting.