Moreover, these data also indicated the presence of a pro-oncogenic pathway activation in glioblastomas, such as the dysregulation of the receptor tyrosine kinase (RTK), Ras and phosphatidyl inositol 3-kinase (PI3K) pathways, via activation of growth factor receptors (EGFR, PDGFRA) and through neurofibromin 1 (NF1) and phosphatase and tensin homolog (PTEN) deletion [23]. This evidence concerns the gene NF1 and glioblastoma.