For example, cancer-associated fibroblasts (CAFs) have been shown to affect tumor cell migration by remodelling the extracellular matrix.[15] Natural killer (NK) and CD8 T cells have been found to take on effector phenotypes and kill tumor cells, whereas myeloid-derived suppressor cells (MDSCs) and Tregs secrete cytokines that suppress the immune system.[4] Further delineation of these complex dynamics in the non-HPV TME is critical for discovering new potential avenues of therapeutic intervention that may drive heterogeneous patient responses to ICI. The gene discussed is CD8A; the disease is neoplasm.