The Cap'n'collar transcription factor BACH1 represses the transcription of gene products involved in oxidative stress protection. Accordingly, agents capable of inhibiting the activity of BACH1 would be of keen interest in treating several autoimmune and age-related diseases. Here, we report that a previously annotated BACH1 inhibitor, HPPE, does not inhibit BACH1 but instead activates a NRF2 driven transcription program that is dependent on the canonical cysteine sensors of NRF2 inhibitory protein KEAP1. Mechanistically, HPPE acts as an ionophore, liberating cellular Zn