The antiapoptotic protein Bcl-2 was found to be overexpressed and critical for leukemogenesis of AML.67 It is frequently overexpressed in leukemia progenitor and stem cells and in myeloid leukemia blasts in comparison to normal hematopoietic cells.68 True to its nature of preventing apoptosis, Bcl-2 has also been shown to play a role in resistance to chemotherapy of AML.69 Based on the importance of Bcl-2, many pharmaceutical companies have developed methods to target Bcl-2 for the treatment of AML. This evidence concerns the gene BCL2 and acute myeloid leukemia.