In order to explore the role of these two pathways of apoptosis during MYC-induced AML, we have overexpressed MYC in HSC, the tumor-initiating cell of AML, either alone or together with cellular inhibitors of the intrinsic or the extrinsic pathways of apoptosis of particular relevance for AML; BCL-XL, BCL-2 and FLIPL. The gene discussed is MYC; the disease is acute myeloid leukemia.