CD8A and neoplasm: Clayton et al. reported that human tumor-derived exosomes express ligands for NKG2D and TGFβ1 that triggered downregulation of NKG2D surface expression by NK and CD8(+) T-cells as an evasion mechanism to avoid their recognition and immune destruction, suggesting that NKG2D is a physiological target for exosome-mediated immune evasion in cancer [34].