Comparing MLL-AF4 binding at promoters genome-wide in both models, we found that MLL-AF4 in CRISPRMLL-AF4+ ALL showed greater enrichment (normalized ChIP-seq reads/bp) at the promoters of infant-ALL- and FL-specific genes compared to MLL-Af4 in CB MLL-Af4+ ALL. Here, KMT2A is linked to acute lymphoblastic leukemia.