Cells of the Ehrlich ascites tumour were fused with A9, A9RI and B82 cells, all three of which were derived from L cells and bore the H-2 k histocompatibility antigen complex and the specific surface antigens associated with the presence of the ‘L cell virion’. In the hybrid cell lines derived from these fusions the expression of both the H-2 k and the specific L cell surface antigens was suppressed in varying degree. This suppression was demonstrated both by the membrane immunofluorescence tests on the cells themselves and by quantitative absorption tests. Hybrid lines derived from the fusion of Ehrlich ascites cells with diploid fibroblasts explanted directly from CBA-T6T6 mice also showed suppression of the H-2 k antigens normally present on the surface of the fibroblasts. When A9 cells were fused with two other ascites tumours, SEWA and MSWBS, which were strain-specific and which bore the H-2 s histocompatibility antigen complex, the resultant hybrid cell lines showed no suppression of the surface antigens characteristic of the A9 cell. These antigens were also fully expressed in hybrids derived from the fusion of A9 cells with normal lymphocytes derived from an ASW mouse. The cells of the Ehrlich ascites tumour thus possess the ability to suppress both the histocompatibility antigens and virus-induced surface antigens contributed to the hybrid cell by the other partner. Hybrids between Ehrlich cells and A9 cells, which, on the whole, have a low level of malignancy, occasionally give rise to highly malignant segregants which show marked chromosomal losses. In some of these malignant segregants, but not in others, the H-2 k antigen complex contributed by the A9 cell, which was initially suppressed in the hybrid, re-appeared. This demonstrates that the absence of the H-2 k antigens in the hybrid cell was due to some suppressive mechanism provided by the Ehrlich component and not to loss of the A9 chromosome bearing the relevant genetic locus. The fact that some highly malignant segregants bear the H-2 k antigen complex and some do not indicates that malignancy and histocompatibility segregate independently.