In KRASG12D-driven pancreatic cancer, KRASG12D promotes glucose utilization via increased expression of glucose transporter 1 (Glut1), hexokinase 1 (Hk1) and hexokinase 1 (Hk2), which induce metabolic flux through GFAT and protein O-GlcNAcylation.30 KRASG12D inactivation, in contrast, downregulated global protein glycosylation, suggesting that KRASG12D-mediated glucose utilization via HBP is essential for O-GlcNAcylation. This evidence concerns the gene HK1 and pancreatic neoplasm.