To explore the relationship between endogenous expression of mutant KRASG12D, a major driver of pancreatic cancer development, and the expression of DUSP5 and DUSP6 we used adenoviral-Cre-mediated recombination in MEFs derived from littermate wild type Kras+/+ (+/+), heterozygous LSL-KrasG12D/+ (G/+) and homozygous LSL-KrasG12D/G12D (G/G) embryos. This evidence concerns the gene KRAS and pancreatic neoplasm.