In pancreatic cancer, initiating mutations in the KRAS gene occur in approximately 95% of patients and are often followed by sequential accumulation of genetic alterations, such as loss of expression, function, or mutations in tumor suppressors and regulators, such as TP53, CDKN2A, INK4A/ARF, and/or PTEN (Bardeesy and DePinho, 2002, Kennedy et al., 2011, Ling et al., 2012, Morran et al., 2014). Here, CDKN2A is linked to pancreatic neoplasm.