As a representative GBM cell line, we used U87MG cells, which is an appropriate model to study the interaction between the AKT/mTOR and MDM2-p53 pathways because of the following characteristics: i) U87MG cells maintain a wild type status of p53, and ii) U87MG cells are deficient for the tumour suppressor phosphatase and tensin homologue (PTEN), a negative regulator of the PI3K/AKT pathway; moreover, PTEN deficiency leads to MDM2 nuclear accumulation, thus inhibiting p53 functions28. The gene discussed is AKT1; the disease is glioblastoma.