In fact, our observations in Bcl-xL/xS, together with the data demonstrating the implication of SF3B1 dysregulation in different oncogenic -pathways that confers drug resistance in GBM (e.g., mTOR-PI3K/cell cycle/DNA -replication, etc.), might be clinically relevant because it has been demonstrated that Bcl-xL is transcriptionally upregulated and associated with poor prognosis and chemoresistance in many cancers [6, 10]. This evidence concerns the gene MTOR and glioblastoma.