KIC mice harbor the two earliest genetic mutations common to most individuals with PDA: oncogenic mutations in Kras, which confer GAP-resistance (e.g. KrasG12D), and deletions of the tumor suppressor Cdkn2a. In the KIC GEMM, neoplasia initiate around 2 weeks of age and tumors (1-2 mm) develop in all untreated mice by P29. The gene discussed is CDKN2A; the disease is Patent ductus arteriosus.