HSCs with heterozygous deletion of Atg5 in a mixed-lineage leukemia–eleven nineteen leukemia (MLL-ENL) mice model showed a high proliferation rate and severe leukemia features with a metabolic shift to glycolysis, an important hallmark for cancer development [119], and also enhanced leukemia features in another MLL-AF9 mouse model [147]. This evidence concerns the gene ATG5 and leukemia.