Moreover, we observed increased BIM levels in the presence of trametinib alone or in combination with ABT-263 (Figure 3k; Supplementary Figure S7e), which could be due to the increased stability of the dephosphorylated form.10 Importantly, the sensitivity of B-ALL cells to ABT-263 was negatively correlated with endogenous levels of BIM and MCL-1 (Supplementary Figures S8a and b), and when MCL-1 was depleted, ABT-263 strongly inhibited B-ALL cell proliferation even in the absence of trametinib (Supplementary Figures S8c and d). This evidence concerns the gene MCL1 and precursor B-cell acute lymphoblastic leukemia.