To detect whether BACH1 accumulation is involved in Fbxo22 deficiency mediated inhibition of AML progression, we crossed Mx1-Cre;Fbxo22fl/fl mice with Bach1+/– mice to generate Fbxo22+/+Bach1+/+, Fbxo22–/–Bach1+/+, Fbxo22+/+Bach1+/– and Fbxo22–/–Bach1+/– mice in the presence of pIpC treatment. This evidence concerns the gene BACH1 and acute myeloid leukemia.