We assume that FcγRIIB-dependent TNFRSF agonist could stimulate immune anti-tumor activities mediated via FcγRIIB expressed on the neighboring macrophages and DCs in tumor microenvironment (TME), with a limited effect on circulating monocytes because of FcγRIIB rareness, which resulted in an optimized efficacy and safety for cancer treatment. Here, FCGR2B is linked to neoplasm.