FDX1 and neoplasm: This binding causes protein aggregation, downregulates Fe–S cluster proteins such as ferredoxin 1 (FDX1), induces protein toxic stress, and triggers programmed cell death.[6] Cuproptosis also functions as immunogenic cell death (ICD), releasing damage‐associated molecular patterns (DAMPs) and tumor‐associated antigens that stimulate immune responses.[7] This mechanism has the potential to reverse the immunosuppressive TME and enhance immune checkpoint inhibitors (ICIs), such as PD‐1 or αPD‐L1 therapies.