Ras is thought to play a major role in the pathogenesis of pancreatic cancer. It normally functions by relaying mitogenic signals initiated by cell surface receptors into the cytoplasm and nucleus. In pancreatic cancer a high incidence of Ras activation by point mutations was found. Activated Ras initiates a cascade of protein kinase activation. These serine/threonine kinases in turn lead to activation of transcription factors localized in the nucleus, which bind to enhancer elements in genes involved in mitogenesis. Experimentally this has been shown by utilizing loss of function mutants of transcription factors which can inhibit Ras-induced transformation. Furthermore there is evidence that these transcription factors can be phosphorylated by these kinases in in vitro assays. These signal transduction pathways should be analyzed in pancreatic cancer and might elucidate new targets for therapy.