Additionally, this combined treatment also largely inhibited TMZ-induced AMPK activation (Fig. 7f, and Supplementary Fig. 11h), RRM1 pT52 levels (Fig. 7g, Supplementary Fig. 11i) and substantially enhanced the levels of γ-H2AX (Fig. 7h, and Supplementary Fig. 11j) and apoptosis in tumor tissues (Fig. 7i and Supplementary Fig. 11k). This evidence concerns the gene PRKAA2 and neoplasm.