Previous studies have shown that the EGFR–PI3K–AKT–mTOR signalling pathway is an upstream regulator of HIF1α; this was verified in our study because we found that EGFR, PI3K and mTOR inhibitors (AG1478, Ly294002 and rapamycin, respectively) restrained HIF1α expression in GBM cells but showed no significant difference in HIF2α expression (Supplementary Fig. S6B). This evidence concerns the gene AKT1 and glioblastoma.