However, either cancer cells under glucose deprivation, hypoxia, or oncogenic KRAS mutation [8] or nontumorigenic pancreatic cells under high glucose levels [10] cause hyper-O-GlcNAcylation of cellular proteins, challenging the regulation of O-GlcNAcylation via the versatile UDP-GlcNAc. The gene discussed is KRAS; the disease is cancer.