Our results not only demonstrated that AZD8055 induced the transient inhibition of AKT in parallel with the feedback induction of EGFR, which is associated with cell resistance to AZD8055, but also disclosed the underlying mechanism by which AKT inhibition released the activity of FoxO 1/3a, which mediated EGFR upregulation in pancreatic cancers. The gene discussed is EGFR; the disease is pancreatic neoplasm.