In addition, the dysregulation of RTK, non-RTK (c-src activity), growth factors (e.g., PDGF, FGF, TGF, and IGF-1), GTPase activating protein (G protein), serine/threonine-specific protein kinase (STK), and NF-κB activity differentially contributes to GBM proliferation [63–66]. The gene discussed is NFKB1; the disease is glioblastoma.