To better characterize the link between the AML-specific role of BRD9 (myeloid immaturity and AML cell growth) and the genomic effects of BRD9 inhibition (reduced chromatin accessibility at cis-regulatory regions and dysregulated transcription), we performed TF accessibility footprinting analysis using our ATAC-seq data through TOBIAS (105). The gene discussed is TF; the disease is acute myeloid leukemia.