The genetic progression model for PDAC, comparable to that of the adenoma-carcinoma sequence seen in colorectal cancer, results from sequential acquisition of mutations in the proto-oncogene KRAS followed by mutations in tumor suppressor genes such as p16/CDKN2A/INK4A, TP53, and SMAD4 that lead to disturbance in cell cycle regulation, and promote the PanIN-to-PDAC progression (Hruban et al., 2000; Schneider and Schmid, 2003). Here, CDKN2A is linked to adenoma.