The distribution of KRAS variant subtypes in our cohort was different than that in other types of cancer, such as lung adenocarcinoma, colon adenocarcinoma, and pancreatic ductal adenocarcinoma (eTable 4 in the Supplement).8 We propose that the KRAS variant patterns are a product, at least in part, of selection during tumor initiation for an ideal level of signaling, which is shaped by the variations in the function of particular KRAS variants, KRAS protein levels, and cellular responses to oncogenic KRAS.8 This evidence concerns the gene KRAS and pancreatic ductal adenocarcinoma.