Although EGFR mutations are present in multiple GBM subsets (based on transcriptional profiles), our tumors most strongly enriched for the human mesenchymal GBM signature (a subtype more responsive to aggressive treatment) [44], likely because the specific cooperative drivers acquired in this model also occur in the human subset (including Nf1, Pten, and Trp53) [44]. This evidence concerns the gene PTEN and glioblastoma.