In pancreas cancer, Eser et al. have shown that PDK1 is an essential effector of KRAS, and that an intact PDK1/PI3K axis is an essential tumor initiating event in cooperation with KRAS for increased cell plasticity, acinar-to-ductal metaplasia (ADM), and pancreatic ductal adenocarcinoma (PDAC) formation [53]. This evidence concerns the gene KRAS and pancreatic neoplasm.