Given that venetoclax (VEN) is an inhibitor specific to BCL2 and some studies have discovered that the level of BCL2 expression is closely related to VEN response in vitro (Souers et al., 2013; Pan et al., 2014), we hypothesized high-UNC93B1 AML might be resistant to venetoclax, and selective MCL1 inhibitor, such as VU661013 (Ramsey et al., 2018), alone or in combination with AZA might be effective in venetoclax-resistant AML and high-UNC93B1 AML. Here, MCL1 is linked to acute myeloid leukemia.