IL- 1β secreted from glioma cells was found to be responsible for the activation of TLR-4 and upregulation of high mobility group box 1 (HMGB1) protein, which eventually results in the increase of HLA-G, a non-classical HLA class I antigen that contributes to glioma immune evasion response [191]. This evidence concerns the gene HLA-G and central nervous system cancer.