In addition, AKT post-translational modification, such as lysine modifications, tyrosine phosphorylation, O-GlcNAcylation, acetylation, and sumoylation are important in retaining AKT hyperactivation in cancers, even in conditions where normal PI3K and PTEN activity persists [1, 117, 118]. The gene discussed is AKT1; the disease is cancer.