ATRi VE822 had the ability to penetrate the blood–brain/tumor barrier and, when combined with olaparib in vivo, abrogated PARPi-induced p-Chk1, increased apoptosis and DNA damage, and extended animal survival in orthotopic GBM models generated from either MYC-amplified or non-Myc GSCs. The gene discussed is CHEK1; the disease is neoplasm.