Although LOH of additional genes within Chr 3p21.1 may contribute to tumor suppression, and loss of BAP1 in pancreatic cancer may be secondary—rather than the cause of genomic instability—our mouse model suggests Bap1 ablation suffices to cause defective DNA repair, pancreatitis, and cooperates with oncogenic Kras to promote pancreatic cancer. This evidence concerns the gene KRAS and familial pancreatic carcinoma.