In addition, the analysis of leukemia reconstituting cells derived from induced pluripotent stem cells from patients with FLT3-ITD/NPM1 suggested an important role for this TF in this AML subtype as well.25 To ensure that our digital footprint-based module construction was valid, we validated binding sites by comparing them to previous ChIP-seq experiments in patients with FLT3-ITD/NPM1 and cell lines1 (Figures S5A and S5B) and found that 79% of genes within the module are RUNX1 ChIP targets (Figure S5B), and 55% of all footprinted sites (Figure S5C) are also bound by RUNX1. This evidence concerns the gene FLT3 and acute myeloid leukemia.