The bispecific mAb induces FcγR-independent but PD-1 dependent GITR clustering in cis, resulting in enhanced activation, proliferation and memory differentiation of primed antigen-specific GITR+PD-1+ T cells along with consequent anti-tumor activity in syngeneic, genetically engineered and xenograft humanized mouse tumor models [56]. Here, FCGR2A is linked to neoplasm.