In glioblastoma, HMGB1 drives glioma stem cell (GSC) formation via the TLR2/NEAT1/Wnt signaling axis, which induces chemoresistance, whereas hypoxia‐induced HMGB1 release activates ERK1/2 signaling through RAGE receptor engagement, thereby enhancing the self‐renewal and proliferative capacity of tumor stem cells [127, 128]. Here, HMGB1 is linked to neoplasm.