In the TME, however, the majority of intratumoral CD8+ and, to a lesser extent CD4+ T cells, expressed markers of antigen-experienced, tissue-resident cells39 and treatment with FcRn-silenced IL-12Fc triggered proliferation of CD4+ effector T cells, a crucial population for anti-GBM efficacy22,33,57. This evidence concerns the gene CD4 and glioblastoma.