FDX1 and neoplasm: On one side, the released Cu2+ could bind to ferredoxin 1 (FDX1) and be reduced to Cu+, while ES could chelate and transport extracellular Cu2+ into tumor cells, resulting in a continuous Cu accumulation to induce cuproptosis.[25] On the other side, Cu2+ could react with GSH and transform into highly toxic Cu+ and GSSG.