Next, to explore whether the metabolic heterogeneity arises from the subsequent mutations during the leukemia development and further confirm our findings in vitro, we overexpressed GFI1B in various AML cell lines, and found that GFI1B overexpression significantly inhibited mitochondrial respiration and shifted metabolic dependence toward glycolysis in THP1, HEL, and OCI/AML3 cells (Supplementary Fig. S9a–c). This evidence concerns the gene GFI1B and leukemia.