Using this sophisticated animal model, we can affirm that pancreatic autophagy, induced during pancreatitis by the overexpression of VMP1, promotes the development of precancerous lesions when induced by the mutated KRAS. In addition, the treatment of these mice with chloroquine, an inhibitor of autophagic flux, reverses the effects of VMP1 in pancreatic cancer induced by the KRAS oncogene. This evidence concerns the gene KRAS and pancreatic neoplasm.