IFNG and neoplasm: Released late in cell death, HMGB1 sustains immune responses via (1) activating DCs to prime tumor-specific T cells; (2) suppressing Tregs to enhance CD8+ T cell cytotoxicity [170,171]; (3) attracting DCs/Th1 cells and regulating DC migration to lymph nodes [172]; (4) binding DC TLR4 to activate NF-κB/IFN pathways, driving pro-inflammatory cytokines (IL-6, IFN-γ) and a positive feedback loop (Fig. 4c) [49,173,174].