For instance, receptor tyrosine kinases, most notably epidermal growth factor receptor (EGFR) and platelet derived growth factor receptor (PDGFR), which are often aberrantly activated in GBM, have been linked to NF-κB activation through a number of mechanisms, involving both protein kinase B/AKT (AKT)-dependent and -independent pathways. The gene discussed is NFKB1; the disease is glioblastoma.