In vivo, CUX1 accelerated pancreatic tumorigenesis by accelerating KRAS-driven development of pancreatic precursor lesions and enhancing development of invasive cancers in two different genetic mouse models in which either full-length CUX1 was expressed under the control of a non-cell type-restricted promoter (CMV) or the p110 CUX1 variant conditionally expressed under the control of a pancreas-specific promoter (Ptf1a). The gene discussed is KRAS; the disease is cancer.