Mice with autophagic defects develop an atypical myeloproliferation resembling MDS progressing to AML (Mortensen et al., 2011); while in our in vitro experiments, increased expression of proteins involved in the autophagy pathway (ATG5, Beclin and LC3B) was connected to long-term exposure to 5-AZA. The gene discussed is MAP1LC3B; the disease is acute myeloid leukemia.