However, the effector functions of NK cells can also be impaired by EVs as the tumor evolves via several mechanisms-including shedding of NKG2D ligand-expressing TEVs that contain MHC class I-related chain A (MICA)*008 and TGFβ1, which induce downregulation of NKG2D on NK cells [248–250]; and direct interaction of TEVs with NK cells, which reduces the expression of perforin and diminishes NK cell cytotoxic activity [251]. Here, TGFB1 is linked to neoplasm.