The results of the present study elucidate that DS/Cu induced apoptosis of B-ALL cells most likely via activation of the mitochondria-related intrinsic apoptotic pathway, reflected by loss of mitochondria membrane potential, down-regulation of anti-apoptotic Bcl-2 family proteins (e.g., Bcl-2 and Bcl-xL), and following caspase-3 activation and PARP degradation. The gene discussed is BCL2; the disease is acute lymphoblastic leukemia.