Given that ADAM10 shedding of immune mediators results in an immunosuppressive microenvironment [96], it is conceivable that exosomal ADAM10 can favor immune privilege in the TME through enhanced shedding of substrates from tumor cells, including NKGD2 ligands, which nullifies NK cell-mediated effector functions [94]. The gene discussed is ADAM10; the disease is neoplasm.