Thus, defects in Lyn, the inhibitory receptors that it phosphorylates in B cells, or the inhibitory phosphatases that become recruited by those inhibitory receptors upon their phosphorylation, all predispose mice to lupus-like autoimmunity, suggesting a critical role for Lyn-mediated attenuation of BCR signaling in preventing autoantibody production to nuclear components. The gene discussed is LYN; the disease is systemic lupus erythematosus.