KRAS and pancreatic neoplasm: In particular, a reduction in glucose utilization through glycolysis and the TCA cycle, favoring hexosamine pathway flux, has previously been described as a possible driver of cell transformation [62], and enhancing total protein glycosylation, in particular the ribonucleotide reductase enzyme, causes an imbalance in dNTP pools, accelerates mutagenesis and the selection of K-RAS-mutated cells and therefore accelerates cell transformation and pancreatic tumors [63].