We used KPC mice that carry K-ras and p53 mutations, leading to early onset of PDA, and KC mice, which have only the K-ras mutation and which show slower progressing lesions and develop PDA later in life.21, 22 As in high-risk individuals, the disease burden in the KC mice increased with time (figure 1), with mice at 2 months having mainly normal tissue (∼60%) and low-grade mPanIN (∼40%), at 4 months mainly low-grade mPanIN and at 9 months equal amounts of low-grade and high-grade mPanIN. The gene discussed is KRAS; the disease is Patent ductus arteriosus.