Specifically, the authors observed that the activation of DRD2 is essential for the proliferation of glioma cells and that the combination of TMZ with DRD2 significantly inhibits GBM cell mitotic activity, increases the induction of DNA double-strand breaks (DSBs), as evident by the formation of γH2aX (a marker of DSBs), and inhibits the autophagic flux caused by TMZ in GBM cells. This evidence concerns the gene DRD2 and central nervous system cancer.