Our findings are in concordance with experimental observations (see Table 1); in a murine pancreatic ductal adenocarcinoma model, the mutated KRAS maintained tumour growth by the stimulation of glucose uptake and channelled glucose intermediates into the hexosamine biosynthesis pathway and pentose phosphate pathway to provide further biosynthetic precursors [59]. The gene discussed is KRAS; the disease is pancreatic ductal adenocarcinoma.