GBP2 inhibited the survival-promoting activity of MCL-1 in AML and CML cells by competitively binding to the BH3 domain of MCL-1, which consequently prevented BAK interaction with MCL-1, and thus the freed BAK readily oligomerized to induce MOMP (Figs. 2, 3d–g and Supplementary Fig. 3). Here, BAK1 is linked to acute myeloid leukemia.