The expression of ber-abl in chronic myelogenous leukemia leads to a large increase in the generation of mature myeloid cells. The key biochemical alteration in this disease is am increased Abl kinase activity. This up-regulation in activity is mediated through the binding of a portion of the Ber molecule to the SH2 regulatory domain of the Ab1 protein. One effect of this alteration is a marked increase in resistance to drug induced cell death by apoptosis. The resistance can be overcome with the use of appropriate antisense oligonucleotides to the bcr-abl gene. The role and contribution of apoptosis to the development of the disease and the prospect of using antisense oligonucleotides as therapeutic agents is discussed.