This subtle phenotype is unique compared to the phenotype of mice deficient for other negative regulators since a defect in CD22 (O'Keefe et al, 1996; 1999; Otipoby et al, 1996; Poe et al, 2000), Lyn (Chan et al, 1998; Hibbs et al, 1995) or SHP1 (Pao et al, 2007), belonging to the same pathway, leads to a common phenotype characterized by increased Ca2+ signaling in B cells after BCR stimulation, a decrease of MZ and mature B-cell populations in spleen and spontaneous production of antinuclear autoantibodies associated with the development of glomerulonephritis. Here, BCR is linked to glomerulonephritis.