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). The gene discussed is SPI1; the disease is acute lymphoblastic leukemia.