Using the online tool PROMO (http://alggen.lsi.upc.es/cgi-bin/promo_v3/promo/promoinit.cgi?dirDB=TF_8.3), we identified TFs which may cooperate in MNX1 activation by binding to E1 (Supplementary Table 5): enriched TF binding sites were found for, among others, GATA and C/EBP family members, which are known to be involved in AML pathogenesis [8]. The gene discussed is TF; the disease is acute myeloid leukemia.