Given that BACH1 promotes ferroptosis by repressing the expression of genes involved in glutathione (GSH) synthesis and iron handling [56], and ferroptosis as well as apoptosis have been shown to act as cancer suppressor mechanism [57], more efforts are required to validate whether BACH1-promoted ferroptosis is also involved in AML progression in the future. Here, BACH1 is linked to acute myeloid leukemia.