It was found to reverse gemcitabine resistance in vitro in pancreatic cancer cell lines by decreasing the expression of MDR-1 (P-gp), NF-κB, and Bcl-2 and increasing the expression levels of Bax, cytochrome-C, and caspase-9 and -3, and promoting cell apoptosis unstimulated and in gemcitabine-induced-resistance pancreatic cancer cell lines [142]. Here, BAX is linked to pancreatic neoplasm.