That is, when KRAS is mutated in pancreatic cancer cells, they signal autonomously to increase cell proliferation via activation of extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) and increased phosphorylation of several kinases such as mitogen-activated protein kinase (MAPK), cyclin-dependent kinase 1 (CDK1) and casein 2 kinase (CKII) [74] (Figure 2a). Here, KRAS is linked to pancreatic neoplasm.