KRAS and pancreatitis: Notably, for normal pancreatic acinar cells, plasticity is an important feature, which means that these cells can recover from ADM to assume normal acinar functions when the self/external pressure (such as pancreatitis and pancreas injury) are removed [40]; however, in the context of Kras oncogene mutation, regardless of whether there is a stimulus present or not, the fate of pancreatic acinar cells is set (irreversible ADM, subsequent PanINs and ultimately PDAC) [41].