(P = 0.0368, P < 0.0001, Figure 4a; P = 0.0097, P = 0.0028, Figure 4b), meantime, patients in the absence of renal disorder had higher serum IFN-λ1 level compared with normal controls as well (P = 0.0258, Figure 4a), but patients without arthritis did not show significant higher serum IFN-λ1 level than normal controls (data not shown), illustrating that IFN-λ1 probably acted in the development of renal disorder and arthritis in SLE. This evidence concerns the gene IFNL1 and arthritic joint disease.