In PAAD, KRAS mutation activates glycolytic signaling mainly through MEK activation and Myc-dependent transcription, resulting in the upregulation of GLUTs and rate-limiting enzymes of glycolysis, such as HK2, phosphofructokinase-1, and lactate dehydrogenase A (LDHA) [37]. Here, MYC is linked to pancreatic adenocarcinoma.