RUNX1 and acute lymphoblastic leukemia: By contrast, this enhancer region was completely void of ATAC-seq signals in ALL samples of other molecular subtypes (TCF3-PBX1, DUX4 rearrangement, ETV6-RUNX1, and KMT2A-AF4), suggesting a causal effect of ZNF384 fusion protein (Fig. 2c bottom panel).