Mechanistically, the reduction of GOT2 in HCC mediated the reprogramming of glutamine metabolism towards the synthesis of reduced GSH, which maintained redox homeostasis in tumor cells by resisting the ROS damage in HCC progression and stimulating the PI3K/AKT/mTOR signaling pathway thereby contributing to the malignant progression of HCC. The gene discussed is AKT1; the disease is hepatocellular carcinoma.