Oncogenic KRAS signals initiate acinar-to-ductal metaplasia, a step essential for the formation of preneoplastic lesions, that together with mutations in tumor suppressors such as CDKN2A, TP53, and SMAD4 occurring during the progression from pre-neoplastic pancreatic intraepithelial neoplasia (PanIN) lesions, promotes the development of invasive cancer.3 Thus, oncogenic mutations in KRAS are necessary to initiate cancer formation and as such remain one of the most studied genetic alterations in PDAC. This evidence concerns the gene KRAS and neoplasm.