FCGR2B and neoplasm: Cumulatively, all of these findings including those made by Wasiuk et al.32 enable us to draw the following conclusions: The therapeutic efficacy of an agonistic immunostimulatory mAb and its mechanism of action is influenced by its isotype and in turn by (1) the abundance of FcγRIIb in the tumour microenvironment, (2) the relative expression of the mAb target on individual cell types, and (3) the reliance of the tumour model on Treg cells, when they express the relevant TNFRSF.