Furthermore, caspase-1 was markedly upregulated by Stefin B overexpression and markedly downregulated by Stefin B knockdown in macrophages (Fig S1B), suggesting that the suppressed mRNA level of caspase-1 in NLRP3 inflammasome observed in Stefin B-treated GA model might be induced by enhanced M2 polarization of macrophages, not directly by Stefin B. These data implied that Stefin B might reduce the release of arthritis-related inflammatory factor IL-17 and repressed the expression of caspase 1 by enhancing the M2 polarization of macrophages, thereby exerting the therapeutic effect on GA. The gene discussed is IL17A; the disease is arthritic joint disease.