This event is triggered by the activation of proinflammatory transcription factors, such as STAT3, NF-kB, and activator protein 1 (AP-1) [10,23,24]; overall it enhances proliferation, invasiveness, or stemness of GBM cells, and it promotes the suppression of tumor-specific immunity [25]. The gene discussed is NFKB1; the disease is glioblastoma.