In an earlier study using a murine model of acute myeloid leukemia (AML), disruption of Clock and/or Bmal1 using RNAi in leukemic stem cells (LSCs) in vivo was shown to produce anti-leukemic effects, including impaired proliferation, enhanced myeloid differentiation, and depletion of LSCs [128]. This evidence concerns the gene BMAL1 and acute myeloid leukemia.