This suggests that while Atm is required for the increased Pdgfra expression in p53ΔN cells, this does not involve alterations in IR or HU-induced Atm signaling, but at this point does not exclude the possibility that increased ROS (reactive oxygen species) levels in p53∆N GBM cells might contribute to Atm pathway activation and subsequent Pdgfra induction and GBM development. The gene discussed is PDGFRA; the disease is glioblastoma.