Since TNFRSF agonist antibodies require crosslinking via Fc γ R and the availability of Fc γ R-expressing cells in GBM, as shown here, is limited, new approaches using dual agonist bispecific antibody targeting CD137 and OX40 in an Fc γ R-independent way, might be of high potential in combination with KIR blockade in the treatment of GBM48. The gene discussed is FCGR2A; the disease is glioblastoma.