GFI1 and acute myeloid leukemia: In summary, the results presented here emphasize that the presence of the GFI1-36N variant in cell lines as well as in a murine model of human AML contributes to DNA damage through alterations in mitochondrial function and metabolism and that this may provide a further explanation for the accumulation of genetic damage and the poorer prognosis of carriers of the GFI1-36N SNP.