The finding that pancreatic tumors which have nuclear CNKSR1 expression in addition to the predominant cytoplasmic expression of CNKSR1 show higher nuclear p-ERK expression levels suggests that cellular localization, rather than absolute CNKSR1 expression levels, might be one of the mechanisms of CNKRS1-mediated control of MAPK pathway activity. This evidence concerns the gene CNKSR1 and pancreatic neoplasm.