Here, we have used chromatin immunoprecipitation followed by high throughput sequencing (ChIP-seq) to identify genome wide NR4A binding sites, and we have integrated these data with gene expression signatures that are acutely regulated upon rescue of NR4A expression in human AML cells to identify direct genomic targets of NR4A1 and investigate its global transcriptional mechanisms of action. Here, NR4A1 is linked to acute myeloid leukemia.