Consistent with this notion, deletions or mutations of p53 [12, 13] or over-expression of Bcl-2 [14, 15] and NF-κB [16] are common in acute myelocytic leukemia (AML) and acute lymphocytic leukemia (ALL) resulting in resistance to drugs that induce apoptosis through the intrinsic pathway. Here, BCL2 is linked to acute myeloid leukemia.