Genetic lesions, including mutations of V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS), cyclin-dependent kinase inhibitor 2A (CDKN2A), tumor protein 53 (TP53), breast cancer 2 (BRCA2), and mothers against decapentaplegic homolog 4 (SMD4/DPC4), have been thought to contribute to the evolution of pancreatic adenocarcinoma [3]. The gene discussed is KRAS; the disease is pancreatic adenocarcinoma.