However, consistent with recent reports showing that antibody-based CD40 activation monotherapy only slightly affects animal survival in syngeneic mouse GBM models, particularly in GL261 models60,61, our study indicates that CD40 antibody treatment alone has no therapeutic efficacy and also fails to sensitize checkpoint blockade therapy in our genetically engineered GBM model, implicating that multiple mechanisms for Mφ activation exist in GBM. The gene discussed is CD40; the disease is glioblastoma.