Another barrier to cuproptosis induction is the overexpression of glutathione (GSH) in tumor cells.[16] GSH can bind to excess Cu(I), forming GSH‐Cu complexes that prevent Cu(I) from triggering cuproptosis in mitochondria.[17] Interestingly, Cu(II) can deplete GSH through reduction reactions, generating Cu(I), which not only binds to ferredoxin 1 (FDX1) to promote cuproptosis but also catalyzes Fenton‐like reactions in the slightly acidic TME.[18] Recently, Cu(II)‐containing nanoparticles (NPs) have emerged as promising reservoirs for copper ions in inducing cuproptosis. Here, FDX1 is linked to neoplasm.