IFNG and neoplasm: The focus of this review is to reposition GBM CAR T-cell therapy as a systems-level issue, turning localized CAR T-cell cytotoxicity into sustained control of the disease by engaging endogenous antitumor immunity via cytokine myeloid chemokine networks.<h4>Methods</h4>We integrated both mechanism- and translation-oriented evidence for how inflammatory mediators derived from CAR T cells (Type I IFNs, IFN-γ, TNF) may license microglia/tumor-associated macrophages for antigen presentation and chemokine secretion, thus recruiting host effector cells and promoting antigen epitope spreading.