RTK II tumors demonstrate greater enrichment for EGFR amplification,12 which, in other cancers, has been shown to maintain intracellular glucose levels through interaction with sodium glucose transporters.38,39 A similar feature may be seen in EGFR-amplified GBM tumors which may preferentially allow RTK II tumors to overcome relatively low ambient glucose levels by actively pumping the substrate into cells. The gene discussed is EGFR; the disease is glioblastoma.