In consistence, Jordan and collaborators found that BCL-2 was upregulated in leukemia stem cells enriched primary AML populations, and that BCL-2 inhibitors (ABT-263 or ABT-737) induced cell death by targeting leukemia stem cell mitochondrial energy generation and showed in vivo therapeutic effects against engrafted primary human AML cells [40]. The gene discussed is BCL2; the disease is acute myeloid leukemia.