Here we mimic the disease etiology of pancreatic cancer in situ, from acquisition of an initiating Kras mutation that occurs in 95% of pancreatic cancers (Biankin et al., 2012, Hingorani et al., 2003) to subsequent loss- or gain-of-function mutations in the tumor suppressor p53, which occur in 50%–75% of pancreatic cancers (Biankin et al., 2012). The gene discussed is TP53; the disease is familial pancreatic carcinoma.