This was achieved by designing an antibody with a 4-1BB binding epitope that depends on FcγR-engagement for its agonistic activity and an IgG4 Fc, which thereby directs the immune activation to the tumor microenvironment where 4-1BB expression is high and there are FcγRs available for Fc engagement and subsequent 4-1BB crosslinking. Here, FCGR2A is linked to neoplasm.