In the context of the TME there have been numerous studies observing that the inhibitory FcγRIIB becomes upregulated on monocytes/macrophages leading to a lowering of antibody-dependent effector capacity(57–60) whilst in contrast enhancing the potential for greater costimulatory agonism.(34) Therefore, the proportions of various myeloid cells in the TME and their relative activating to inhibitory FcγR levels will influence the mechanisms by which agonist mAb stimulate an anti-tumor response. This evidence concerns the gene FCGR2A and neoplasm.