Therefore, these data provide original, compelling evidence that SF3B1 is functionally linked, likely via SRSF1 modulation, to these well-known relevant pro-oncogenic pathways (AKT-mTOR/ß-catenin) in GBM, which further supports the pathophysiological relevance of SF3B1 and the antitumor actions of SF3B1-blockade in GBM. The gene discussed is AKT1; the disease is glioblastoma.