As shown in Figure 1c, the level of p62/SQSTM1, an LC3-interacting protein degraded in the autolysosomes, was increased in response to AICAR in accordance with previously published results that demonstrated p62/SQSTM1 upregulation during differentiation of AML cells.17 In addition, to check for targets downstream of AMPK, phosphorylation of Ulk1 on Ser555 as a trigger for mTOR-independent autophagy was examined in cells treated with differentiation agents. The gene discussed is MAP1LC3A; the disease is acute myeloid leukemia.