By utilizing two different transgenic mouse models expressing p200 CUX1 or p110 CUX1, respectively, and crossbreeding these mouse lines with KC (KrasLSL-G12D/+; Ptf1aCre/+) mice expressing KRAS in a pancreas-specific manner, we identified p110 CUX1 as major driver of mPanIN progression and pancreatic tumor formation in the context of activated Kras. Here, KRAS is linked to pancreatic neoplasm.