While AKT inhibition alone induced a CD62L+ central memory–like phenotype with impaired tumor-resident and effector functions in CAR-T cells, AKT inhibition in combination with RUNX3 overexpression improved cytotoxic potential and tumor infiltration in a pancreatic ductal adenocarcinoma model (105). Here, AKT1 is linked to pancreatic ductal adenocarcinoma.