While these two reports did not explore the mechanism of disease exacerbation, we propose that it overlaps with the resistance or susceptibility to induced autoAb production mediated by the S378N G-CSFR polymorphism, and that the B6.Sle2c2 and B6.TC strains offer an excellent model to identify the cellular and molecular bases on how G-CSF modulates SLE pathogenesis. The gene discussed is CSF3; the disease is systemic lupus erythematosus.