Inflammation underlies disease development, as shown by deletion of the proinflammatory cytokine interleukin (IL)‐6, which prevented lupus nephritis, while the mice remained autoimmune‐prone.15, 16 G‐CSF levels have been found to be elevated in the serum of aged Lyn−/− mice in settings where the mice were engineered to show augmented tissue inflammation and disease such as in the context of IL‐10 deficiency17 or when Lyn was deleted specifically from DCs.18 The gene discussed is CSF3; the disease is lupus nephritis.