MRL mice bearing the lpr (Fas) or gld (Fas ligand) mutation, MRL‐Fas^lpr or MRL‐FasL^gld , respectively, develop arthritis similar to rheumatoid arthritis, but C3H and C57BL/6 mice bearing such mutations do not. In MRL‐Fas^lpr mice, agalactosylated oligosaccharides in serum IgG increase significantly in comparison to MRL‐+/+ mice without arthritis. In this study, an increased level of agalactosylation in IgG, as compared to MRL‐+/+, was found in both MRL‐Fas^lpr and MRL‐FasL^gld mice. In contrast, the incidence of IgG without galactose was comparable among C3H‐Fas^lpr , C3H‐FasL^gld , and C3H‐+/+ mice as well as between C57BL/6‐Fas^lpr and C57BL/6‐+/+ mice. These results suggest that the increase in agalactosylated IgG and the development of arthritis in MRL‐Fas^lpr and MRL‐FasL^gld mice are controlled by the MRL genetic background.