Lyn-deficient mice were generated to analyze the role of Lyn in B cell antigen receptor (BCR) signaling. These mice had a reduced number of peripheral B cells with a greater proportion of immature cells and a higher than normal turnover rate. Aged lyn^−/− mice developed splenomegaly, produced autoantibodies, and had an expanded population of B lymphoblasts of the B1 lineage. Splenic B cells from young lyn^−/− mice initiated early BCR signaling events, although in a delayed fashion. Unexpectedly, lyn^−/− B cells exhibited an enhanced MAP kinase activation and an increased proliferative response to BCR engagement. Stimulation of lyn^−/− B cells with intact and F(ab′)₂ anti-IgM revealed defects in at least two mechanisms that negatively regulate BCR signaling, one of which involves FcγRIIb1.