A review spotlights copper overload as a driver of cuproptosis—a mitochondria-dependent cell death pathway—and frames it as a potential cancer vulnerability. The piece summarizes how excess copper pushes tumor cells toward cuproptosis and notes a strategy of combining copper-targeting approaches with immunotherapy. The major biotech relevance is mechanistic: cuproptosis offers a defined, druggable intersection between metal metabolism and mitochondrial stress, potentially distinct from apoptosis-centric paradigms. That differentiation could translate into alternative sensitization strategies and improved response durability. For pipeline builders, the review serves as a target biology map—connecting copper regulation, mitochondrial machinery, and combination rationale toward immuno-oncology contexts.