Additionally, results of co-immunoprecipitation and immunofluorescence revealed that fenretinide promoted the interaction between NR4A1 and Bcl-2, which exposed the BH3 domain of HL-60 cells, indicating that the NR4A1-mediated conformational changes in Bcl-2 might be involved in the fenretinide-caused apoptosis effect on AML cells. This evidence concerns the gene NR4A1 and acute myeloid leukemia.