Furthermore, our data revealed a potential utility of SF3B1 as aggressiveness biomarker in GBM which is supported by the direct and strong association found between SF3B1 expression levels and relevant development/progression tumor -markers (e.g., MKI67/PDGFRA) [59] and different oncogenic spliceosome components, including SRSF3 (the most critical splicing machinery component in GBM recently identified by our group) [23], in human GBM and tumor -samples from EPed-glioma mouse models. This evidence concerns the gene MKI67 and neoplasm.