Cancer cells reprogram their metabolism at many levels to meet the high demand for ATP and metabolites necessary for rapid tumor growth. We recently showed that inactivation of ZBTB7A, a transcription factor essential for lineage fate decision, causes upregulation of glycolysis culminating in increased energy supply in myeloid leukemia cells (Redondo Monte et al., 2020, Oncogene). ZBTB7A mutations are specifically associated with AML t(8;21), pointing toward cooperation with the RUNX1-RUNX1T1 fusion. However, the underlying mechanism is still not fully understood.