GBM on the other hand showed a very high genomic alteration frequency in EGFR (46%) and negative regulators of KRAS and PI3K, NF1 (8%), and PTEN (26%), making KRAS and its downstream effector PI3K/AKT a targetable driver of GBM (Figure 5F) (Excel Sheet 2, sub-sheet S2.1). The gene discussed is EGFR; the disease is glioblastoma.