Moreover, our data indicate that pladienolide B inhibitory actions observed in AKT-mTOR/ß-catenin signaling pathways may likely be exerted through a significant down-regulation in SRSF1-levels, a relevant pro-oncogene overexpressed in GBM [1, 13, 23, 71, 74] which acts activating both signaling pathways simultaneously [22, 64]. The gene discussed is MTOR; the disease is glioblastoma.