In Complex karyotype AML, co-treatment with venetoclax and pegcrisantaspase, an asparaginase, significantly diminished cellular protein synthesis including that of MCL-1, an important antiapoptotic protein in AML, by promoting the interaction between eIF4E and 4EBP1 on the cap-binding complex and interfering with active cap-mRNA translation downstream of mTOR signaling[75]. This evidence concerns the gene ASPG and acute myeloid leukemia.