We found that (a) pancreatic cancer cells activated the PI3K/Akt pathway against cisplatin treatment; (b) inhibition of the PI3K/Akt pathway enhanced the antitumor effect of cisplatin, and (c) cisplatin induced apoptosis with subsequent deactivation of proapoptotic factors such as Bad and Caspace-3. This evidence concerns the gene AKT1 and pancreatic neoplasm.