We have previously shown that AML blast cells with FLT3-ITD and FLT3-ITD/NPM1 mutations display a specific chromatin signature distinct from healthy CD34+ cells.1 To construct GRNs, we then integrated transcriptomic (RNA-seq), HiC, and digital footprinting data based on high-resolution DNaseI-seq experiments.2 The comparison between the GRNs of normal and malignant cells identified TF families showing FLT3-ITD+ AML-subtype-specific interactions with their targets, which could be attributed to aberrant expression of genes promoting AML survival. The gene discussed is TF; the disease is acute myeloid leukemia.