Knock-down of PER1 induced apoptosis and resulted in the upregulation of Bax and downregulation of BCL-2, highlighting its potential interest as a target in pancreatic cancer gene therapy [4].The overexpression of pro-apoptotic genes such as BAX and TRAIL also showed antitumoral effects and sensitization to gemcitabine chemotherapy [5]. Here, BAX is linked to pancreatic neoplasm.