AKT1 and neoplasm: As c-MYC, including via the PI3K/Akt/mTOR/c-MYC pathway [122], is sufficient to upregulate O-GlcNAc and OGT in tumours, whilst mTORC1-induced c-MYC and its induction of LAT-1 are core aspects of glycolytic metabolism, changes driven by O-GlcNAcylation are integral aspects of the alterations in metabolism classically associated with tumours, namely glycolysis upregulation and the limited maintenance of OXPHOS.