FCGR2A and neoplasm: Subsequent pre-clinical studies showed that for optimal activity in mice, mIgG1 can directly activate costimulatory receptor expressing CD8s when sufficient inhibitory FcγRIIB is present on tumor myeloid cells, whereas mIgG2a/c are most effective when target expression is high on intratumoral Treg and activating FcγR dominate the TME (73–75).