AKT1 and neoplasm: Mechanistically, ITGB2 upregulates the PI3K/AKT/mTOR pathway and activates glycolytic activity in CAFs.[45, 46, 47, 48, 49] Taken together, these findings provide preliminary evidence that ITGB2 mediates crosstalk between tumor cells and CAFs, creating a TME that favors tumor progression.