Furthermore, tumors driven by distinct Akt isoforms were characterized by pronounced differences in gene and protein expression: Of note, a particularly high expression of DNA repair protein-encoding genes like polymerase delta 1 (PolD), DNA polymerase epsilon (PolE), Exonuclease 1 (EXO1), Proliferating cell nuclear antigen (PCNA), and Flap endonuclease 1 (FEN1) were observed in Akt3-derived high-grade glioma and might explain their increased resistance to radiotherapy and chemotherapy [8]. Here, FEN1 is linked to glioma.