Abstract Ferroptosis is a form of regulated cell death characterized by iron-dependent phospholipid peroxidation and is closely related to various diseases. System Xc−, a cystine/glutamate antiporter, and glutathione peroxidase 4 (GPX4) are key molecules in ferroptosis. Erastin and RSL3, known as inhibitors of system Xc− and GPX4, respectively, are commonly used as ferroptosis inducers. Broad-Complex, Tramtrack and Bric a brac (BTB) and Cap‘n’collar (CNC) homology 1 (BACH1), a heme-binding transcription repressor, promotes pro-ferroptotic signalling, and therefore, Bach1-deficient cells are resistant to ferroptosis. Irikura et al. (Ferroptosis model system by the re-expression of BACH1. J. Biochem. 2023;174:239–52) constructed Bach1-re-expressing immortalized mouse embryonic fibroblasts (iMEFs) from Bach1−/− mice, which induce ferroptosis simply through the depletion of 2-mercaptoethanol from the culture medium. Transcriptional repression by re-expressed BACH1 induces suppressed glutathione synthesis and increases labile iron. Furthermore, ferroptosis initiated by BACH1-re-expressing iMEFs is propagated to surrounding cells. Thus, the BACH1-re-expression system is a novel and powerful tool to investigate the cellular basis of ferroptosis.