By contrast, other SLAMF receptor-deficiencies embedded in the BALB/c genome, such as Slamf1−/−(BALB/c.129) and Slamf2−/−(BALB/c.129), do not develop any autoimmune response (25), underscoring the role played by Ly9 as a negative regulator in the pathogenesis of lupus. The gene discussed is SLAMF1; the disease is systemic lupus erythematosus.