Chronic lymphocytic leukemia (CLL) is the most common human leukemia, accounting for ~10,000 new cases diagnosed each year in the United States and representing ~30% of all leukemia cases [1]. CLL patients can often survive for a number of years showing relatively mild symptoms [1]. Indeed, a significant proportion of CLL cases are diagnosed incidentally. CLL leukemic cells usually show morphologically mature appearance and usually do not proliferate in vitro [1, 2]. This disease occurs in two forms, aggressive and indolent, both forms are characterized by the clonal expansion of CD5 positive B-lymphocytes [1, 2]. For the most part aggressive CLL is characterized by high ZAP-70 expression and unmutated IgH VH, while indolent CLL shows low ZAP-70 expression and mutated IgH VH [1, 2]. For a number of years it was generally accepted that CLL is caused by an inherent defect in apoptosis, and that malignant lymphocytes accumulate due to diminished cell death [1, 2]. Consistent with this theory, CLL cells are relatively inert, do not proliferate, and accumulate until levels not supportable by a patient. However, this original view
