For the treatment of AML, MLN4924 dramatically disrupted AML cells growth, inhibit clone formation, and decreased Cullin-dependent substrates expression, causing the inhibition of NF-κB transcriptional activity and increased reactive oxygen species (ROS) generation.565 However, there are different biological mechanisms of MLN4924 in distinct genetic subgroups of diffuse large B-cell lymphoma (DLBCL). Here, CACUL1 is linked to acute myeloid leukemia.