TNF-α allows glioma cells to evade the immune response and to destructively expand in the inflammatory microenvironment by increasing both the expression of the major histocompatibility complex class (MHC-I) and its transcriptional activation (in parallel with amplified hypoxia-inducible factor 1-alpha (HIF-1α), ΝF-κΒ, and β-catenin actions) [52]. This evidence concerns the gene HIF1A and central nervous system cancer.