Further proof that K-ras mutations represent an initiating event in PDAC comes from mouse models, in which expression of a mutant activated K-ras allele (K-rasG12D) in pancreatic epithelium is sufficient to induce the formation of both PanIN lesions and invasive pancreatic cancer, pathologically resembling the human disease [3]. The gene discussed is KRAS; the disease is pancreatic neoplasm.