The reliance on several dysregulated—and often redundant—signaling pathways, including EGFR, PIK3CA, PDGF, and NF-κB, has been well-characterized in glioblastoma, and cross-talk between these have likely contributed in large part to the historical failures of targeted therapy [53,145,146]. This evidence concerns the gene NFKB1 and glioblastoma.