Investigations of the somatic genomic landscape of GBM’s demonstrated a connection between gene alteration and signaling pathway modifications in GBM cells, which include receptor tyrosine kinases (RTK) pathways (EGFR1, FGFR2 or PDGFRA), PI3K/PTEN-AKT-mTORC1 pathway, MAPK pathways, p53 pathway, RB1 pathway (RB1, CDK4 and CDK6) [9, 13] and IKK-NF-κB pathway with frequent inactivation of inhibitor kappa-B (NFKBIA) [14, 15]. The gene discussed is FGFR2; the disease is glioblastoma.