The current standard of care for glioblastoma (GBM) is surgical resection plus postoperative radiotherapy. tolerance to radiotherapy in GBM is a difficult clinical problem. Previous studies have suggested that GBM cells show upregulation of hypoxia-inducible factor 1α (HIF1α) and pyruvate dehydrogenase kinase 1 (PDK1) in the presence of inadequate blood supply, which leads to increased glycolysis and radiotherapy tolerance. Dichloroacetate (DCA), an inhibitor of PDK, alters tumor metabolism, restores the oxidative phosphorylation process in tumor cells, reverses anaerobic glycolysis of GBM, and improves GBM radiotherapy sensitivity. The main purpose of Shen et al. study was to verify that radiotherapy promotes glycolysis and that DCA reverses the glycolytic process to enhance the sensitivity of GBM to radiotherapy. In an in vitro experiment, the expression of glycolysis-related genes was detected to be up-regulated in U87GBM cells treated with radiation, and the isoenzyme of PDK was increased 1.26-3.38-fold. westernblot results showed that HIF1α was also up-regulated simultaneously. Glycolysis was significantly reduced in DCA-treated tumor cells after radiotherapy (P < 0.01). dCA inhibited the proliferation of GBM cells, which led to a decrease in the mitochondrial reserve function of tumor cells; induced an increase in reactive oxygen species and promoted apoptosis. All of the above mentioned alterations contributed to improve the sensitivity of tumor cells to radiotherapy. Then in vivo animal experiments were performed. After injection of U87GBM cells in the right basal ganglion of nude mice, they were divided into 4 groups: no treatment group, radiotherapy alone group, DCA alone group and radiotherapy combined with DCA group. Whole brain irradiation was performed 13 days after tumor implantation at a total dose of 20 Gy in more than 10 fractions. The proliferation of tumor cells was assessed by HE staining and Ki-67 staining, etc. The results revealed that tumor proliferation was significantly inhibited in the radiotherapy combined with DCA group, and the survival of the tumor-bearing mice was significantly prolonged. In conclusion, DCA is a small molecule that can enter the blood-brain barrier, and it modulates the glucose metabolism pathway in the brain to make tumor cells more sensitive to radiotherapy, thus improving the effectiveness of radiotherapy. The study by Shen et al. shows that DCA can alter the glucose metabolism of tumor cells without harming normal brain tissues and improve the effect of standard treatment in GBM patients, providing a new idea for the treatment of GBM.