Another common feature is that mutations of the Kras gene are found in > 90% of human pancreatic adenocarcinoma tumors [34–36] as well as in > 95% of PanINs have been reported to have Kras mutations [37] and the Ptf1a-Cre; LSL-KrasG12D mouse model was constructed to cause activation of PanIN initiation and pancreatic tumor formation based on the introduction of the G12D Kras mutation with activation restricted to expression in the pancreatic tissue [4], presumably mimicking spontaneous somatic cell Kras mutations that occur in the initiation of human pancreatic cancer [28, 37]. The gene discussed is PTF1A; the disease is familial pancreatic carcinoma.