HMGB1 and glioblastoma: Because TLR4 is one of HMGB1 receptors, and TLR4 could regulate phosphatidylinositol 3 kinase (PI3K)/Akt signaling pathway and induce cytokine secretion through mitogen-activated protein kinase signaling [26–28], it was therefore speculated that TREM2 might mediate the development of GBM radioresistance and immune escape through HMGB1/TLR4/Akt signaling pathway, siTREM2s were then transfected into GBM cells to verify this hypothesis.