Notably, the CAR gene modification of CIK cells did not inhibit their original MHC-unrestricted antitumour activity which is principally mediated by the interaction between NKG2D and stress-inducible molecules such as MHC class I-related chain A and B (MIC A/B) and UL-16-binding proteins (ULBPs) expressed on the surface of tumour cells10. This evidence concerns the gene HLA-C and neoplasm.