Eser and colleagues showed that hat PDPK1 is an essential effector of Kras, and that an intact PDPK1/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) formation39. This evidence concerns the gene PDPK1 and neoplasm.