BACH1 inhibits the survival of AML cells by downregulating HO‐1.[447] FBXO22 promotes AML progression by degrading BACH1, and overexpression of BACH1 suppresses AML progression.[448] Bortezomib (Btz), a proteasome inhibitor, is clinically effective in multiple myeloma (MM) but ineffective in AML. This evidence concerns the gene BACH1 and acute myeloid leukemia.