Other possible mechanisms for tumor recognition are through receptors from the natural cytotoxicity (NCR) family like NKp30 (31), the DNAM1/DNAM-1 receptor-ligand recognition (32, 33), and receptors from the NK receptor family like the mentioned NKG2D-receptor that recognized “stressed” or malignant transformed cells by activation through MHC-class I-related molecules MIC-A and MIC-B (6, 34) and UL16-binding proteins (ULBPs) (35, 36). This evidence concerns the gene CD226 and neoplasm.