Upon implantation of chemical carcinogen DMBA or transgenic expression mutant Kras in pancreatic acinar cells, rpS6p−/− mice (knockin mice lacking all five phosphorylatable sites in rpS6) couldn’t develop pancreatic cancer precursor lesions [40], indicating that rpS6 phosphorylation is essential for tumorigenesis. This evidence concerns the gene RPS6 and pancreatic neoplasm.