Specifically, cuproptosis-induced mitochondrial proteotoxic stress promotes the release of mitochondrial DNA (mtDNA), which acts as an intracellular DAMP,320 activating the tumor-immune-related mtDNA-cGAS-STING signaling pathway and leading to the secretion IFN-β and CXCL10.321 Subsequently, these cytokines facilitate DC maturation, cytotoxic CD8+ T cell infiltration, and natural killer (NK) cell recruitment, collectively promoting tumor regression in preclinical models. The gene discussed is CXCL10; the disease is neoplasm.