IL-35 dysregulation may have multifunctional roles in the pathogenesis of infection, its stimulation may reduce the concentrations of IFN-γ, IL-1β, IL-6 and IL-8 produced by peripheral blood mononuclear cells, indicating antiviral immunity inhibited by IL-35 in HBV infection, with a reduction in the secretion of pro-inflammatory cytokines (Table 1) in peripheral blood mononuclear cells co-stimulated by HBsAg and IL-35, decreased STAT1 phosphorylation also occurs.43 The gene discussed is IFNG; the disease is infection.