In addition, crosstalk between pancreatic acinar cells and neoplastic lesion in the pancreas occurs via substitution of a single base in Kras; moreover, Philip et al. [227] further well documented that high lipid diet activated the Kras via COX2 followed by an inflammatory response in the pancreas with stromal fibrosis, neoplastic lesion in the pancreas and pancreatic ductal adenocarcinoma from normal acinar cells of the pancreas [227]. This evidence concerns the gene KRAS and pancreatic ductal adenocarcinoma.