Canonical NF-κB signaling, typically based on IKKβ-dependent phosphorylation and degradation of IκBα, enabling p65/p50 nuclear translocation, and non-canonical signaling, NIK-IKKα-dependent processing of p100 to p52/RelB, are both engaged in glioma, integrating cytokines (e.g., TNFα, IL-1β), DAMPs, and receptor tyrosine kinase activity [38,39]. This evidence concerns the gene NFKB1 and glioma.