In contrast, we showed that suppression of mitochondrial fusion by MFN2 or OPA1 knockdown induced the differentiation of leukemic blasts, and that MFN2 depletion reduced both leukemia initiation and self-renewal in AML PDX assays in vivo, suggesting that the block in G0 phase induced by mitochondrial fusion inhibition did not result in a “stem-like” phenotype of quiescent cells in AML. The gene discussed is MFN2; the disease is leukemia.