Major histocompatibility complex (MHC) class I molecules can function as specific target antigens in T-cell-mediated cytotoxity ^1,2. In addition, T cells can kill target cells through non-MHC antigens, for example, virally infected cells, if the target and effector cells express the same MHC class I antigens². Consequently, quantitative and/or qualitative variations in the expression of the H–2/HLA antigens on the target cells could interfere with MHC-restricted immune reactions. We have reported that the AKR leukaemia cell line K36.16, a subline of K36 (ref. 3), on which the H–2K^k antigen cannot be detected, is resistant to T-cell lysis and grows very easily in AKR mice⁴. Other AKR tumour cell lines, like 369, which have a relatively large amount of H–2K^k on their surface, are easily killed by T cells in vitro and require a much larger inoculum to grow in vivo⁴. Monoclonal antibodies against H–2K^k, but not against H–2D^k, prevented the killing by T cells^4,5. This suggests that some tumour cells grow in vivo because tumour-associated antigen(s) cannot be recognized efficiently by the host's immune system, due to the absence of MHC molecules which would function as restriction elements for T-cell cytotoxicity. We have tested this hypothesis by introducing the H-2K^k gene into the H–2K^k-deficient AKR tumour cell line K36.16 and have now demonstrated directly the biological relevance of H–2K^k antigen expression in the regulation of the in vivo growth of this tumour cell line.