In the present study, we tested the effect of targeting Akt using the pan-Akt inhibitor MK-2206, which inhibits all three isoforms of Akt, with the intention of impeding the migration and radiation resistance of two GBM cell lines differing in p53 and PTEN status [44], and therefore exhibiting different background expression of PI3K pathway proteins, including Akt. The gene discussed is TP53; the disease is glioblastoma.