A direct support for this mechanism comes from a study applying a knockdown of anti-apoptotic mRNAs for BCL-2, BCL-XL, and MCL-1 or using a BCL-2 family inhibitor (GX15-070) in pancreatic cancer cells with combined administration of SAHA or sodium valproate and sorafenib; these inhibitory agents induced autophagy and intrinsic apoptosis, thus bypassing extrinsic apoptosis resistance [318]. This evidence concerns the gene BCL2 and pancreatic neoplasm.