NR4A3 and acute myeloid leukemia: Such an explanation can reasonably explain why AML would develop in mice with concurrent abrogation of NR4A1 and NR4A3. In addition, the assignment of NR4A1 as a class I aberration and NR4A3 downregulation as a class II aberration suggests that the double-knockout animal model might faithfully recapitulate key aspects of the myeloid leukemogenesis process in humans, and it could be an excellent explorative model for further AML research.