Furthermore, TUSC2 expression and erlotinib treatment increase intracellular ROS, promoting cell death, and further addition of the thioredoxin reductase 1 inhibitor, auranofin, further increases cellular ROS, inhibits colony formation, and increases lung cancer apoptosis, suggesting that these therapies may be appropriate for lung cancer patients that exhibit TUSC2 loss with concomitant alterations in EGFR or AKT activity [34,38,43,73]. This evidence concerns the gene AKT1 and lung carcinoma.