To provide further evidence for the role of increased acetylation at GFI1/LSD1-bound enhancers as a critical mediator of drug-induced myeloid differentiation, we co-treated THP1 AML cells with OG86 and the active enantiomer of the BRD2/3/4 bromodomain inhibitor JQ1. Here, GFI1 is linked to acute myeloid leukemia.