Two important pathways mediate part of this resistance in these tumors: PTEN/Akt/PI3K pathway, which is over activated in GBM cells through loss of PTEN, over expression of EGFR (a typical alteration of primary gliomas) and/or increase of PI3k/Akt activity due to mutations in its regulators; and NF-κB pathway, which is constitutively activated in a large proportion of GBMs and is increased by cells in response to cytotoxic drugs, favoring cell survival by inducing the expression of anti-apoptotic genes. The gene discussed is AKT1; the disease is glioblastoma.