All G12, G13, and Q61 mutants are gain‐of‐function, leading to constitutively active KRAS protein and dysregulated downstream signaling; for example, the mitogen‐activated protein kinase MAPK and PI3K‐AKT signaling cascades of KRAS mutants in G12D and G12V are present in 60%–70% of pancreatic ductal adenocarcinomas (PDAC) and 20%–30% of colorectal cancers (CRC) [7, 8, 14]. This evidence concerns the gene KRAS and pancreatic ductal adenocarcinoma.