The researchers established that activating KrasG12D mutation and Lkb1 inactivation led to IPMN, primarily of the gastric type, and shared some characteristics with human IPMN.[53] These findings imply that IPMN initiated due to mutant KRAS is controlled by oncogenic GNAS activation and LKB1 inactivation. The gene discussed is GNAS; the disease is pancreatic intraductal papillary-mucinous neoplasm.