AKT1 and gastric cancer: In particular, activation of PI3K/Akt enhances glucose uptake and glycolysis.[41, 42] This increases the expression of glucose transporters on the cell surface, activating hexokinase and capturing intracellular glucose via phosphorylation, leading to increased lactate conversion for glycolytic glucose metabolism and the promotion of cell growth, division, and metastasis.[20, 43, 44] Our results showed that ECAR and glycolysis‐related proteins increased with DEPTOR upregulation and Akt activation in GC cells.