An interesting hypothesis underlying the fasting-induced sensitization of 4T1 breast cancer cells to chemotherapy is that the decrease of glucose, IGF-1, and other progrowth signals dictates increased consumption of energy as well as generation of ROS due to paradoxical activation of the AKT/S6K, partially via the AMPK-mTORC1 energy-sensing pathways malignant cells. The gene discussed is AKT1; the disease is breast cancer.