The genetic background of PDAC is well known and INK4a/ARF (p16), TP53, DPC4/Smad4 tumor suppressor pathways are genetically inactivated in the majority of pancreatic carcinomas (associated with losses of heterozygosity of, respectively, 9p21, 17p, and 18q), whereas oncogenic Kras is activated [15,16,17]. Here, CDKN2A is linked to neoplasm.