BCL2 and acute myeloid leukemia: These cells do not over-express the anti-apoptotic protein BCL-XL.[24] Of the other BCL-2 family prosurvival members MCL-1 has the shorter half-life (approximately 1 hour) and can be rapidly downregulated [38] whilst BCL-2 is a much more stable protein.[37, 39] We used etoposide and AC220, as DSB-inducing agents and FLT3 inhibitors are of particular clinical interest in AML: both rpS6 dephosphorylation and dynamic BH3 profiling had been able to predict response to these drugs (S1 Table).