Since JNK was originally identified as a kinase activated by Ras [32, 33], and given that K-Ras is mutationally activated in more than 90% of pancreatic ductal adenocarcinoma [34, 35], we first sought to determine whether K-Ras has a role in the control of JNK signaling in pancreatic CSCs/CSLCs. Here, KRAS is linked to pancreatic ductal adenocarcinoma.