Of note, while erlotinib was not as effective at inhibiting p-EGFR, p-ERK, and p-AKT in the other two GBM PDXs tested, the combination of erlotinib and MLN0128 profoundly inhibited p-EGFR, p-AKT, p-ERK, and p-RAS40 levels in both GBM197 (Figure 2d) and GBM218 (Figure 2e). This evidence concerns the gene AKT1 and glioblastoma.