In characterizing these patterns, we also identified leukemic dependencies that may be amenable to inhibition or targeting, including Prmt1, Hdac3, Setdb1 and Kmt2d. Furthermore, we identified that these altered roles relate to leukemia-specific transcription factor–chromatin factor interactions, including COMPASS and BAF factors that rewire their transcription factor networks toward Runx and Stat transcription factors (Fig. 7d). Here, SOAT1 is linked to leukemia.