The soluble and/or membrane-bound forms of FasL have been detected in most NKEVs (6, 11, 15) and are thought to act via distinct mechanisms including classic receptor–ligand interaction involving the membrane receptor FasL expressed on NK92 cell-derived exosomes, which exhibits time- and dose-dependent cytotoxic effects on melanoma cells (8); and the endocytic pathway, whereby NKEVs containing soluble FasL is taken up by target cells and interacts with intracellular structures to induce FasL-mediated cell death (6). This evidence concerns the gene FASLG and melanoma.