Inhibition of mitochondrial translation, mitochondrial chaperonin, CLPB or even mitophagy regulator, FIS1 (Mitochondrial Fission 1 protein) and its upstream target AMPK leads to loss of LSC self-renewal potential, myeloid differentiation, and cell cycle arrest and ultimately cell death even for the resistant AML LSCs (26–28). The gene discussed is FIS1; the disease is acute myeloid leukemia.