Research conducted on mice have shown that the reduced or even complete knockout of expression of Dicer accelerates KRAS-driven acinar dedifferentiation and leads to the loss in the polarity of cluster cells, which initiates both epithelial-to-mesenchymal transitions (EMT) and cluster metaplasia to ductal, a process that has been shown to precede and promote the formation of pancreatic cancer precursors [60]. This evidence concerns the gene KRAS and familial pancreatic carcinoma.