Thus, in addition to increased levels of “free” BH3-only protein(s) (i.e. unbound by anti-apoptotic proteins) resulting from BCL-2 inhibition by venetoclax, and/or alvocidib reduction of MCL-1 protein, alvocidib may have the capacity to induce apoptosis by increasing total BIM protein levels and/or other BH3-only proteins, although this activity was not observed in our small sampling of AML analyzed ex vivo (n = 4). The gene discussed is BCL2L11; the disease is acute myeloid leukemia.