PU.1-deficient B-ALL cells also harbored reduced H3K27ac at Bim –117 and reduced Bim mRNA levels, suggesting that PU.1 is responsible for maintaining this enhancer in an active state while, paradoxically, also facilitating TRIM33 recruitment (Figure 3F and Figure 3—figure supplement 3). Here, BCL2L11 is linked to acute lymphoblastic leukemia.