The results confirmed that the expression of β-catenin, c-Myc, p-GSK-3β and LEF1 were upregulated in GBM cells in presence of HMGB1, and silencing TLR2 by siRNAs could attenuate this effect (Figures 6B,C), suggesting that HMGB1 activated Wnt signaling via TLR2. This evidence concerns the gene HMGB1 and glioblastoma.