Increased BCL-2 activity, as well as dysregulation of further members of the BCL-2 signaling cascade, has previously been shown in acute lymphoblastic leukemia (ALL) and other hematological malignancies like acute myeloid leukemia (AML), chronic lymphoblastic leukemia (CLL), chronic myeloid leukemia, several lymphomas, or myeloma [2, 5]. This evidence concerns the gene BCL2 and B-cell chronic lymphocytic leukemia.