For example, in pancreatic ductal adenocarcinoma, which is highly dependent on KRAS signaling, G12A remains a notably rare variant, representing roughly 0.8% of KRAS-mutant tumors, whereas in non–small cell lung cancers, G12A accounts for a more substantial proportion, reported at approximately 10% of KRAS-mutant cases [5,7,8,31]. The gene discussed is KRAS; the disease is pancreatic ductal adenocarcinoma.