Our findings are consistent with a non-leukaemic PuER model of Pu.1-/- cells, where a relatively small group of CEBPB peaks were observed after PU.1 induction with strong enrichment for PU.1 motifs, and were co-bound by PU.1 in over 75% of cases.36 CEBPA co-localisation to existing PU.1 peaks was also noted in a recent study of RUNX1-ETO knockdown in a t(8;21) AML cell line.54 This evidence concerns the gene SPI1 and acute myeloid leukemia.