These immunosuppressive TAMs can subsequently shape the immunosuppressive tumor microenvironment and promote immunotherapy resistance in GBM through mechanisms such as (i) secreting immunosuppressive cytokines (e.g., IL-6, IL-10, TGF-β) (ii) promoting T cell exhaustion, and (iii) secreting chemoattractant to recruit regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) [40, 41], as indicated by previous literature. Here, IL10 is linked to neoplasm.