Even though current epigenomic glioma classification [48] was unavailable for our large cohort of retrospective specimens which in turn have adequately extensive clinical follow-up data associated, our results strongly support our pharmacological approach of inhibiting the SOX9–STAT3–PML axis as a new therapeutic strategy in GB, at least for a subset of patients originated from the transformation of NSCs, for mesenchymal subtype or with high levels of SOX9, STAT3 and/or PML. Here, PML is linked to central nervous system cancer.