Previous studies suggested interactions of Olig2 with the DNA damage pathway: Olig2-mediated proliferation and glioma stem cell propagation is achieved by repression of CDKN1A,30–32 which is a downstream target of DNA damage induced p53 activation and regulates cell cycle progression.33,34 As high-throughput analyses after dnE47 activation showed significant alterations of the KEGG pathways cell cycle, Fanconi anemia and p53 pathway and their commonly shared ATR–CHK1 pathway, this builds a very promising basis for ATR inhibition as a potential therapeutic concept in glioma therapy. The gene discussed is TP53; the disease is glioma.