Occupied TF binding motifs as determined by digital footprinting within such sites were then assigned to a TF family.2,11 Such regions were assigned to promotors using previously determined promoter-capture HiC (CHiC) interactions from a FLT3-ITD+ AML sample or the nearest gene (both within 200 kb of the promoter).2 RNA-seq was used to identify genes specifically upregulated in the FLT3-ITD+ AML subtype compared to healthy CD34+ cells (>2 FC, p < 0.1). Here, TF is linked to acute myeloid leukemia.