Although heterozygous Bach1 loss in Fbxo22+/+ cells did not accelerate MLL-AF9-induced leukemogenesis, heterozygous Bach1 loss in Fbxo22–/– cells partially but significantly reversed delayed leukemogenesis in Fbxo22–/– mice, as evidenced by percentages of GFP+ AML cells in peripheral blood mononuclear cell (PBMC), BM and blast cells in BM, sizes and weights of spleen/liver and tissue infiltration with leukemic cells (Fig. 7B–E). The gene discussed is MLLT3; the disease is acute myeloid leukemia.