BCL2 and acute myeloid leukemia: By performing this assay on AML cell lines and primary blasts, A. Letai’s Lab at the Dana-Farber Cancer Institute, Boston, USA, showed that AML blasts were primed for BCL-2, (i.e., BCL2 inhibition lowered the threshold to apoptotic induction), whereas normal HSC were less sensitive to BCL-2 inhibition [27,29,30].