Although a number of driver mutations have been identified in PDAC tumors in addition to several tumor suppressors [CDKN2A (cyclin-dependent kinase inhibitor 2A), TP53 (tumor protein p53)] and the predominant KRAS (Kirsten Rat Sarcoma) mutations, the percentage of patients with therapeutically targetable mutations is low [2]. The gene discussed is KRAS; the disease is neoplasm.