Cancer-cell mitochondrial dysfunction (e.g., altered OXPHOS, elevated mtROS, mtDNA release, or mitochondrial transfer to immune cells) reshapes the tumor microenvironment toward immunosuppression by promoting regulatory myeloid phenotypes, impairing antigen presentation, and blunting CD8+ effector functions include mechanisms that have been linked to poorer immune checkpoint inhibitor (ICI) outcomes (258). Here, CD8A is linked to neoplasm.