For example, within the fructose-rich milieu of acute myeloid leukaemia (AML), malignant blasts upregulate GLUT5.3 This permits the uptake of fructose, which then enters glycolysis and is subsequently channelled into serine and proline biosynthetic pathways during blast proliferation.4 Increased tumour cell metabolism and dysregulated perfusion can create competition for nutrients. This evidence concerns the gene SLC2A5 and acute myeloid leukemia.