The changes in RTK, PI3K, TP53, cell cycle, neoangiogenesis, cellular metabolism, NF-κB [10], signal transducer, and activator of transcription 3 (STAT3) [14, 15] signaling pathways have already paved the way for considering them as feasible targets in GBM [10, 16, 17]. The gene discussed is NFKB1; the disease is glioblastoma.