Combining our findings with previously described CFL1-dependent mechanisms, we postulate that although inactivation of AKT and STAT3 in response to CFL1 knockdown would normally lead to CYCS release and subsequent activation of caspases in pancreatic cancer cells, BAX activation is prevented by lack of availability of unphosphorylated CFL1, thus counteracting apoptosis induction in this case. Here, STAT3 is linked to pancreatic neoplasm.