First, it is possible that autophagy pathways independent of LC3 lipidation could have a compensatory role in this model of AML.38, 39 Studies have shown that mice lacking Atg5 or Atg7 in HSCs demonstrate temporary myelomonocytic proliferation with aberrant maturation.9, 13 In this model of MLL-AF9-driven AML, LSCs resemble immature myelomonocytes.2, 4, 40 A separate study has already suggested that myeloid cells might rely on Atg5-independent autophagy for survival and differentiation.41 Second, MLL-AF9 expression might attenuate autophagy's role as a tumor suppressor by inactivating p53. The gene discussed is MAP1LC3A; the disease is acute myeloid leukemia.