Indeed, cross-linking of CD16 with rituximab (anti-CD20) has been shown to induce SHP-1-dependent hypo-responsiveness of NK cells to a diverse array of activating signals, including third-party tumor cell lines and cross-linking of NKp46, 2B4, NKG2D, and DNAM-1 (32). Here, NCR1 is linked to neoplasm.