Previous studies have also demonstrated that CEACAM6 overexpression in gastric cancer (GC) cells increased apoptotic resistance to 5‐FU,15 while gene silencing of CEACAM6 in pancreatic ductal adenocarcinoma BxPC3 cells resulted in improved sensitivity to gemcitabine through modulation of AKT activity in a Src‐dependent manner.16 This evidence concerns the gene AKT1 and pancreatic ductal adenocarcinoma.