In theory, besides being an apparent critical pan-antibody regulator conferring antibody drug resistance in the tumor microenvironment, targeted blockade of FcγRIIB by a separate antibody has the advantage of enabling combination therapy and boosted efficacy with multiple existing, clinically validated, antibodies including those engineered for enhanced binding to activating FcγR (65). This evidence concerns the gene FCGR2A and neoplasm.