This research suggested a possible role for FcγRIIb in the detrimental effect associated with anti-PD-1 therapy, and concluded that this phenomenon is maintained by myeloid cells, such as M2-like tumour-associated macrophages (TAM), within the TME by FcR-dependent mechanisms probably through inhibitory receptors (141). The gene discussed is FCGR2B; the disease is neoplasm.