It was demonstrated in SV40-transformed human fibroblasts [131] and glioblastoma cells [132] that hypoxia-induced AMPK activation resulted in the enhancement of both the expression/activation of Ataxia telangiectasia-mutated (ATM) and the activation of DNA-dependent protein kinase catalytic subunit (DNA-PKCs)—two enzymes contributing to DNA double-stranded break repair. The gene discussed is ATM; the disease is glioblastoma.