By exposing AML cell lines and primary blasts from R/R AML patients to the BCL-2/BCL-XL/BCL-W inhibitor ABT-737, they were able to demonstrate the disruption of BCL-2/BAX association, resulting in the freeing up of BAX and BIM, which, in turn, leads to cytochrome c release, caspase activation, and finalization of the apoptotic cascade. The gene discussed is BCL2L1; the disease is acute myeloid leukemia.