The authors reported that the T3-treated GBM cells were arrested at the pre-G1 phase, which was accompanied by DNA damage and a concomitant increase in Caspase-8, BCL-2 Associated X (Bax), and BH3 interacting-domain death agonist (Bid) levels as well as the cytosolic release of cytochrome c [33]. This evidence concerns the gene BAX and glioblastoma.