The striking predominance of PanINs over IPMNs in our model may be due to a dosage effect, where IPMN formation requires complete loss of Arid1a in ductal progenitors or ductal cells, while acinar cells expressing mutant Kras are more highly dependent on Arid1a to maintain their identity, and thus are rapidly reprogrammed to mucinous PanINs upon partial Arid1a suppression. Here, ARID1A is linked to pancreatic intraductal papillary-mucinous neoplasm.