Combinations (at levels shown to be non-cytotoxic to normal human fibroblasts or human peripheral blood mononuclear cells) inhibited the growth of, and induced apoptosis in, HL-60 and KG-1a human acute myeloid leukemia cells. Proposed mechanism of action: Apoptosis associated with activation of caspases 8, 9 and 3 and Bid (a proapoptotic protein) which is a member of the Bcl family. No other Bcl proteins shown to be affected. No evidence that oxidative stress was involved. Here, BID is linked to acute myeloid leukemia.