In addition, an attempt has been made to focus on signal transduction pathways such as the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), the Janus kinase/signal transducer and activator of transcription (JAK/STAT), the mitogen-activated protein kinase (MAPK), the phosphatidylinositol-3-kinase/Akt/ the mammalian target of rapamycin (PI3K/Akt/mTOR), and Toll-like Receptors (TLRs), which are activated during neuroinflammation, further supporting the role of inflammation in GBM progression and maintenance. The gene discussed is NFKB1; the disease is glioblastoma.