Recent evidence positions transketolase (TKT) as a central orchestrator of this metabolic rewiring: clinical specimens and established AML cell models exhibit substantially upregulated TKT levels, which facilitate cellular expansion, invasive capacity, and metabolic adaptation through transcriptional control of ribokinase (RBKS), creating a positive regulatory loop that amplifies non-oxidative pentose phosphate flux and promotes epithelial–mesenchymal transition phenotypes. The gene discussed is TKT; the disease is acute myeloid leukemia.