Since activating mutations in the Epidermal Growth Factor Receptor (EGFR) and the inactivation of the Phosphatase and TENsin homolog (PTEN) are recurrent in de novo GBM [12], the most used model showed the co-activation of EGFR and PI3K (PTEN antagonist) in glial cells, resulting in the formation of neoplastic tumors with cells acquiring the ability to proliferate and invade [13]. The gene discussed is PTEN; the disease is glioblastoma.