Several mechanisms have been proposed for how T2A inhibits GBM growth, beyond PI3K/PKB/mTORC1 signalling, including through the inhibition of STAT3 and increased activation of death receptors [13, 16] or through upregulation of neural lineage marker expression [3], but further mechanistic insight may provide new approaches for GBM treatment. The gene discussed is STAT3; the disease is glioblastoma.