Upon glucose deprivation, PERK/eIF2α/ATF4 axis induced the transcription of FUT1 which in turn activated AKT/mTOR/4EBP1 pathway through targeting glycoproteins such as including CD147, ICAM-1, EGFR, and EPHA2, resulting in enhanced stem-like property of HCC [68]. The gene discussed is MTOR; the disease is hepatocellular carcinoma.