BCL-xL/BCL-2 inhibitor navitoclax consistently showed potent in vitro activity against an extended panel of primary and PDX ALL samples (mean IC50 = 7.8 ± 4.6 nM, n = 17 Fig. 4A); concentrations well below clinically reported plasma levels following oral administration of navitoclax in humans (Cmax = 4–6 μM) [26, 27]. This evidence concerns the gene BCL2L1 and acute lymphoblastic leukemia.